Module 15 - Pharmacotherapy For Ophthalmological Disorders

Geriatric
Pharmacy Review Module 15 Pharmacotherapy for Ophthalmological Disorders
Accreditation Information
ASCP is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
This home study web activity has been assigned 3 credit hours. ACPE UPN: 0203-0000-10-008-H01-P Release Date: 2/17/2010 Expiration Date:2/17/2013
To receive continuing education credit for this course, participants must complete an on-line evaluation form and pass the online assessment with a score of 70% or better. If you do not receive a minimum score of 70% or better on the assessment, you are permitted 4 retakes. After passing the assessment, you can print and track your continuing education statements of credit online.
Geriatric Pharmacy Review courses have not yet been approved for Florida consultant pharmacy continuing education.
Copyright 2011 American Society of Consultant Pharmacists
Content Experts
Current Content Expert: Charlie Waters, PharmD, BCPS, CGP Clinical Manager Cardinal Health
Legacy Content Experts: J. William Doyle, MD, PhD College of Medicine University of Florida Mary Fran Smith, MD College of Medicine University of Florida
Disclosures: Charlie Waters, PharmD, BCPS, CGP has no relevant financial relationships to disclose. J. William Doyle, MD, PhD has no relevant financial relationships to disclose. Mary Fran Smith, MD has no relevant financial relationships to disclose.
Degenerative Diseases of the Elderly Eye
Learning Objectives:
By the end of this review concept, you should be able to: Describe the basic intraocular pressure and aqueous humor dynamics of the human eye.
Explain the pathophysiological changes that can occur in the elderly eye, specific to dry eye, cataracts, and macular degeneration. Examine and apply patient, disease, and medication-related factors influencing the choice of treatment intervention for degenerative diseases of the eye. Review the effects of systemic diseases on the eye.
Age-related Changes in the Eye
Decrease in tear production Drooping eyelids (ptosis) Corneal decompensation (natural i.e. Fuchs dystrophy, or post surgical) Atrophy of iris and ciliary muscles Opacity in the crystalline lens Liquefaction, cavitation, detachment of vitreous Degenerative processes of retina (age related macular degeneration) Damage to the retina by other diseases of aging Damage to the optic nerve by diseases of the elderly, i.e. glaucoma, vasculopathy
Age-related Changes in the Eye
Natural age-related changes to the eye account for most of the ophthalmological disorders seen in elderly patients. These changes are usually bilateral, symmetrical, and typical for each age group. Some of the more common changes include a decrease in basal tear production, dry lids from loss of oily secretions resulting in decreased vision and discomfort, thinning of the conjunctiva, and discoloration of the sclera. Sclerosis of the lens substance, causing blurred vision, and decreased elasticity of its capsule contribute to loss of accommodation. Degenerative diseases can affect the retina such as age related macular degeneration and the loss of sharp acuity. Also, many systemic diseases, such as diabetes, or hypertension, can damage the retina and cause profound visual loss. Lastly, the optic nerve is susceptible to diseases in the elderly such as glaucoma or arteriosclerosis and infarction.
Signs and Symptoms of Dry Eye Syndrome

Conjunctival injection Unhealthy cornea Dry or scratchy feeling in the eye Impaired vision Poor blink Foreign body sensation Pain and intermittent epiphora
Dry eye syndrome, which results from an age-related decline in tear production, is an important cause of disability in the elderly. The absence of tears can lead to problems such as conjunctival injection, an unhealthy cornea, and impaired vision. Patients often complain of a foreign body sensation. The tear film is necessary for sharp vision and to help nourish the corneal epithelium. When it fails, vision blurs and the eyes become irritated and painful. Often a reflex tearing causes the eye to well up with tears and have epiphora.
Risk Factors for Dry Eye Syndrome
Elderly Female Any surface trauma i.e., burns Connective tissue disease Long term use of medications such as for glaucoma Multiple surgeries Exposure (Bells palsy) Thyroid disease Steven Johnson syndrome Sjgren's syndrome Lupus Neurotrophic keratitis Meibomitis Medications (especially anticholinergics) Elderly persons are more likely to experience dry eye syndrome and females more often than males. Other patients who are particularly at risk for dry eye syndrome include burn victims individuals with connective tissue or persons on long term use of medications such as for glaucoma, persons who have undergone multiple surgeries, patients with Sjgren's syndrome ( an immune system disorder ), and a disease known as "neurotrophic keratitis" and some types of contact lens wear may decrease sensitivity of the cornea. All of these conditions can decrease the basal tear production rate and lead to dry eyes. Moreover, persons with infection and inflammation of the meibomian glands in the eyelids and those who suffer from thyroid disease, may also experience dry eye syndrome caused by excessive evaporation of tears. Certain use of medications such as antibiotics, antihistamines, diuretics, and anti-diarrheas, may dry up the mucous membranes and cause dry eye syndrome.
Treatment of Dry Eye Syndrome

There are a multitude of over-the-counter tear preparations for dry eye which range from then to very viscous Bottled Tears with Preservatives: Polyvinyl alcohol 1% (Hypotears) thin Polyethylene glycol 2%/dextran 1% (AquaSite) thicker Generic (usually 3% methylcellulose) Individual use, preservative-free tears: Carboxymethylcellulose 1% (Celluvisc) thick Carboxymethylcellulose 0.5% (Cellufresh) fairly thin Bottled tears with degradable preservative: Hydroxypropyl methycellulose (GenTeal) Polyvinyl alcohol (Refresh) Ointments: Petrolatum/mineral oil (Lacrilube) Polyvinyl alcohol (Refresh PM) Treatment of Dry Eye Disease: Cyclosporine (Restasis) Initially, dry eye syndrome is best treated through the use of polyethylene glycol solutions. These solutions contain preservatives for the occasional user. Individual use, preservative-free tears are more expensive, but are recommended for patients who require daily treatment for the entire year. Newer, less expensive bottled tear products contain a preservative that breaks down after application, so the preparation is effectively preservative-free. Ointments are usually reserved for bedtime use, especially in patients with lagophthalmos. However, ointment application during the day may be an option for patients with severe dry eye. Cyclosporine (Restasis) is now available. It decreases T-cell mediated inflammation of the conjunctiva which has been shown to decrease basal tear productions. The diseases most likely to be helped by this are keratitis sicca, Sjogrens, and dry eye secondary to collagen vascular diseases. Patients who remain symptomatic despite the use of medication should consult their eye specialist about closing the tear drain.
Degenerative Diseases of the Lens and Retina
Diseases of the Lens Cataracts
Primary diseases of the Retina Age related macular degeneration (AMD) Retinal detachment Vitreous detachment Systemic diseases that affect the retina Diabetes (edema, exudates, neovascularization, hemorrhage) Hypertension (exudates, increased risk of vascular occlusions) +HIV (micro infarcts, opportunistic infections)
Degenerative diseases of the lens and retina account for many of the ophthalmological disorders seen among the elderly. Cataracts, the most common disorder of the crystalline lens, may be caused by trauma, toxicity, metabolic disorders, or, most commonly, the aging process itself. The vision is completely restored by cataract extraction and artificial lens implantation. Diseases of the retina have more profound and possible permanent visual loss. Age related macular edema can cause irreversible loss of central vision. Vitreal detachment usually is a benign condition, but may lead to retinal detachment, where the sensory retina separates from the photoreceptor layer. This leads to permanent loss if not surgically repaired. Lastly, many diseases affect the eye, with diabetes being the most common. The changes can range from minimal to profound, usually as a function of length of disease and tightness of sugar control.
Effects of Cataracts on Vision
Impairment of near vision Impairment of far vision Sensitivity to glare outdoors Monocular diplopia (from cleft or vacuole) Lens swelling and refractive changes
The increasing opacity characteristic of cataracts may impair vision in a variety of ways. Some cataracts impair far vision, while others impair near vision. Some patients will become hypersensitive to glare, while others will acquire monocular diplopia. Transient refractive changes due to lens swelling may even provide temporarily vision improvement in some patients.
Steps in Cataract Extraction (Phacoemulsification)
1. Incision 2.8 3.2 mm 2. Use of ultrasound to break up cataract and remove debris from eye 3. Insertion of foldable implant into eye 4. Closure using single or no stitch 5. May be done under topical or local anesthesia
Surgical removal of the cataract is the only effective treatment. The majority of cataract extractions are accomplished using Phacoemulsification and small incision techniques. Once the incision is made, ultrasound is used to break the cataract into dust and remove debris from the eye. A foldable implant is inserted, and the incision is closed. The patients resume their normal activity faster as compared to conventional extracapsular surgery, which involves larger incision (10-12mm) that may take 6-8 weeks to heal and stitches for closing that may cause distortion of the normal curvature of the cornea leading to astigmatism and blurred vision.
Pre-operative Preparation for Cataract Extraction
Topical, antibiotic drops for 1-3 days prior to surgery Topical NSAID 1 day prior to surgery (esp. in DM patients) Possible discontinuation of prostaglandin analogs for glaucoma
Preoperative preparation for cataract surgery includes use of topical, antibiotic drops for one to three days prior to surgery. Some physicians will prescribe a topical non-steroidal anti-inflammatory drug a day prior to surgery, especially with diabetic patents. If the patient is taking a topical prostaglandin analog for glaucoma, especially latanoprost, it should be discontinued several weeks prior to surgery, due to increased risk of post-operative cystoid macular edema.
Post-operative Management for Cataract Extraction Topical Antibiotics
Administration: BID QID x 7 10 days Treatment Options: Gatifloxacin (Zymar ) and moxifloxacin (Vigamox ) are 4th generation fluoroquinolones Even broader spectrum and little risk of allergy Ofloxacin, ciprofloxacin, 3rd generation fluoroquinolones Broad spectrum coverage, little risk of allergy Trimethoprim-polymyxin B (Polytrim ) oncreased allergy risk Gentamicin, tobramycin Cheaper
Monitor for: Development of antibiotic toxicity
Post-operative management of the patient includes the administration of topical antibiotics two to four times a day for seven to ten days. Zymar and Vigamox provide excellent broad spectrum coverage, and the 3rd generation fluoroquinolones are also very effective, and carry little risk of allergy. The risk of allergic reaction is increased with alternative medications. With any of these regimens, patients should be monitored for antibiotic toxicity.
Post-operative Management for Cataract Extraction Anti-inflammatory Drugs
NSAID drops Flurbiprofen (Ocufen ), diclofenac (Voltaren ), ketorolac (Acular ) QID Decreased risk of post-op macular swelling ADRs - corneal irritation Topical Steroids Dexamethasone, prednisolone QID q2h (depending on case) x 2 4 weeks ADRs - corneal toxicity, increased intraocular pressure (IOP) as soon
as 1 week after initiation
Treatment of post-operative inflammation in the cataract extraction patient may be accomplished by using drops of a nonsteroidal anti-inflammatory drug four times a day. Flurbiprofen, diclofenac, and ketorolac are often used because they also decrease the risk of macular swelling. Topical steroids may be used instead of or in addition to the drops. Dexamethasone or prednisolone may be given four times a day up to every two hours for two to four weeks. Both nonsteroidal anti-inflammatory drugs and topical steroids may produce adverse effects on the cornea.
Post-operative Red Eye
Because of the risk of post-operative complications, the cataract extraction patient must be watched carefully for red eye and other symptoms. Red eye can be a result of initial surgical insult and operative subconjunctival injection of steroids or antibiotics. It can also be a sign of postoperative inflammation or antibiotic toxicity. In rare occasions, red eye can signal an intraocular infection, a potentially disastrous complication that requires immediate medical evaluation. Emergent physician referral is a must whenever patients present with red eye, swollen lids, or discharge following cataract extraction.
Incidence of Macular Degeneration
Incidence of Macular Degeneration Leading cause (15 million Americans) of irreversible blindness in persons over 60 years Average age of onset: 65 years Second eye usually involved in < 4 years
Macular degeneration is one of the most important retinal diseases in the aged. It is the leading cause of irreversible blindness in persons over the age of 60. The average age of onset is sixty-five, with the second eye usually becomes involved within four years. There is no treatment to cure macular degeneration, but options now exist to lessen the visual impact.
Pathogenesis of Macular Degeneration
Detachment of retinal epithelium and loss of the close association of the photoreceptors and ganglion cells of the retina Sub retinal and choroidal neovascularization Rupture and hemorrhage of new vessels with possible atrophic scarring Possible macular hole due to retinal thinning Loss of central vision
There are two types of macular degeneration; "wet" or neovascular and "dry" or atrophic. Macular degeneration is caused by the build up of degenerative products such as hyalin from photoreceptors concentrated in the macular area. Exudative detachment of the epithelium follows, often accompanied by neovascularization of the choroid. Rupture and bleeding of the new vessels in the area can cause sudden total loss of central vision. Repair of tissue in the macular area may produce atrophic scars. Thinning of the retina may result in macular hole.
Clinical Signs of Macular Degeneration
Decline in visual acuity, with or w/o loss of reading vision (20/400) New onset of metamorphopsia (distortion) New para central blind spot View the Progression of Macular Degeneration Symptoms as seen through the eyes of the patient: http://www.ahaf.org/macular/about/Macular_ProgressionNEW_FLASH.htm
Since the area affected may vary in size and discreteness, patients in the early stages of macular degeneration may still have good visual acuity. Some patients will begin to lose their reading vision. Clinical signs that should trigger referral to a physician include a recent decline in acuity, the onset of metamorphopsia, or a new paracental blind spot.
Management and Treatment of Macular Degeneration
Vitamins with zinc and selenium Antioxidants Laser surgery for patients with neovascularization Photodynamic therapy Continued ophthalmic care with follow-up tests (acuity, Amsler grid)
Although there is no known treatment for macular degeneration, vitamins with zinc and selenium may be helpful in slowing its progression. For the twenty percent that develop neovascularization, laser surgery may prevent hemorrhage and further damage. Photodynamic therapy has been very effective in preventing profound visual loss with wet macular degeneration. Verteporfin (Visudyne) is injected IV in the arm, and it binds to the endothelium of the neovasuclar vessels. Upon shining o bright light, it chemically reacts and seals off the new blood vessels with little or no collateral damage to surrounding normal cells. The patient must be warned that they, too, will be very photosensitive for 24 hours and avoid contact with sunshine. For patients with large confluent drusen or early AMD, vitamins with antioxidants, zinc and selenium have been shown to slow down the progression of the disease. No evidence shows that these vitamins are preventative for ARMD. Follow-up for macular degeneration should include acuity tests and Amsler grid. Continuing ophthalmic care is a must.
Diseases That Affect the Eye: Diabetes
Diabetes Affects the small blood vessels of the entire body The eyes and kidneys are most involved Causes intra-retinal microaneurysms, exudates, and hemorrhage Can cause clinically significant macular edema and loss of acuity If ischemia persists, neovascularization occurs with development of new abnormal blood vessels Neovascularization most commonly occurs at the optic nerve head, retina or iris, which may lead to glaucoma Eventually, vitreous hemorrhage, tractional retinal detachment and blindness will occur without treatment
Diabetes, both insulin and non-insulin dependant forms, can greatly affect the eye and vision. Since diabetes affects the smallest blood vessels in the body, the most common organs affected are the eye and the kidney. Microvascular defects occur with subsequent hemorrhage, exudates and ischemia of retinal tissue. This decreases the function of the retina and vision loss occurs. In the case of clinically significant macular edema, the swelling decreases the acuity. Laser treatment to the macula (focal laser) has been shown to improve the acuity and delay further loss. If significant retinal ischemia occurs due to the microvascular damage, the eye grows new blood vessels, neovascularization. They most commonly occur at the optic nerve head, posterior retina or iris. If this occurs on the iris, they may block the trabecular meshwork and neovascular glaucoma develops. If unchecked, this leads to vitreous hemorrhage, tractional retinal detachment and blindness. With the use of lasers and surgery when necessary, the ophthalmologist can slow or arrest this process and prevent or delay vision loss. Ophthalmologic care is a necessity for all patients with diabetes.
Diseases That Affect the Eye: Hypertension
Hypertension Arteriosclerosis causes increased risks of vascular occlusions, especially branch or central retinal vein occlusions Also increased risk of ischemic optic neuropathy as the vessels feeding the optic nerve become occluded Central retinal artery occlusion can occur from arteriosclerosis or emboli from calcific plaques from the carotid arteries Increased risk of stroke and if the occipital cortex is involved, then vision loss from cortical damage occurs
High blood pressure also affects all the blood vessels of the body, with the eye being sensitive to the changes. As the wall of the arterioles thickens with the elevated pressure, the veins, which share a common sheath, become compressed. The risk of venous occlusion increases with duration of the hypertension. Also, the very small arterioles that feed the optic nerve are susceptible to occlusion with elevated blood pressure. Emboli from the carotid arteries can cause central retinal artery occlusions and profound or complete visual loss. Many of these changes are preventable if the blood pressure is kept under adequate control.
Resources
For additional information, see: Douglas, R., Jr., Cullom, B., & Chang.(1994). The Wills eye manual: Office and emergency room diagnosis and treatment of eye disease, 2nd ed.Philadelphia:Lippincott-Raven. Fechner, P.U. & Teichmann, K.D. (1998).Ocular therapeutics: Pharmacology and clinical application.Slack. Hammond BR Jr, Johnson MA.The age-related eye disease study (AREDS).Nutr Rev. 2002 Sep;60(9):283-8. Kelly, J.S., (1993).Visual impairment among older people. Brit J Nurse, 2(2): 110-6. Kertes, P. & Conway, M. D. (Eds.).Clinical trials in Ophthalmology: A summary and practice guide.William & Williams. Lavali, M. M., Hollyfield, J. G. & Anderson, R. E. (Eds.). (1997).Degenerative retinal diseases.Plenum. MacCumber, M. W., (Ed.). (1997).Management of ocular injuries and emergencies. Philadelphia:Lippincott-Raven. American Academy of Ophthalmology, EyeNet Karolinska Intitutet Library, Eye Diseases New York University, Department of Ophthalmology: Digital Opthalmic Slide Collection http://www.ahaf.org/macular/about/maabout.htm http://www.agingeye.net/otheragingeye/blepharitis.php#
Infections
By the end of this Review Concept you should be able to: Identify common sites of ophthalmological infection and their corresponding disorders. Describe the etiology, pathogenesis and clinical features of blepharitis, conjunctivitis, and corneal and uveal tract infections. Outline recommended management and treatment strategies for common ophthalmologic infections.
Common Infections of the Eye
DISORDER Blepharitis Conjunctivitis Corneal disease / ulcers Cellulitis Uveitis Lids
SITE
Conjunctiva Cornea Orbits Uveal tract
Infections can occur in virtually every part of the aging eye. Infection of the lid margin, or blepharitis, is common in the elderly and is usually associated with seborrhea of the surrounding eyebrow and skin areas. The decline of tearing and other defensive mechanisms predispose elderly patients to infections of the conjunctiva. Corneal ulcers occur as a result of bacterial, viral, or fungal infection. Frequently, they occur with use of aphakic contact lenses or other surface disruptions, as may be caused by surgery. Cellulitis is usually a result of bacterial infection of the orbit usually after trauma. While uveitis is an inflammatory disorder not normally associated with infection, inflammation of the uvea can be caused by herpes infection, or other blood bourn pathogens, especially in the immunocompromised patient.
Etiology and Pathogenesis of Blepharitis
Cause: Seborrheic infection of lid margins and miebomian gland openings Clinical Course: Lid margins become red and thickened Ectropion and flaking develop Entropion and trichaisis can also occur Corneal scarring may occur from lashes rubbing against cornea Complications: Secondary Staph infection with sties, ulcerations, chalazia and abscesses
Blepharitis is a chronic, annoying, and sometimes disabling and disfiguring disease in which the lid margins become red and thickened. They may develop ectropion or entropion and are dusted by fine, dandruff-like flakes. Corneal scarring may result from the rubbing of the lashes against the cornea. Secondary staphylococcal infections can occur with sties, corneal ulceration, chalazia and abscesses. Marginal keratitis is a corneal opacity/ulcer caused by an immunological process from Staph antigens.
Clinical Signs and Symptoms of Blepharitis
Clinical Signs and Symptoms of Blepharitis Burning Scratching / foreign body sensation Itching Tearing Possible sensitivity to light, smoke, or dust Cracking at the canthi
The patient with blepharitis often presents with, burning, scratching, sandy or gritty sensation, itching and/or tearing. He or she may complain of intolerance to light, smoke and dust. Since wrinkled skin tends to retain moisture and tears, the patient often experiences cracking and further irritation of the canthi or lower lid. It can be mistaken for "dry eye" due to the gritty sensation that may occur, however lubricating drops do little to improve the condition.
Treatment of Blepharitis
Warm compresses for 15 minutes q12h x 1 2 weeks, then qhs Gentle baby shampoo (diluted) for lid scrubs Artificial tears Erythromycin or combination antibiotic / steroid (Blephamide) eye ointment qhs Doxycycline po for 1 month
Treatment of blepharitis is usually a life-long affair. Treatment is frequently initiated with lid scrubs, using a gentle diluted baby shampoo, and erythromycin or antibiotic/steroid combination ointment. Oral doxycycline is used for recalcitrant cases. Warm compresses and massage of the lash margin at bedtime may need to be continued for years.
Common Conjunctival Infections and Their Causes
Catarrhal conjunctivitis -secondary Staph Gram-negative infections - chronic dacryocystitis or contaminated contact lenses Adenoviral conjunctivitis virus Herpetic infections (HSV and Zoster)
Infection is but one of the many causes of conjunctival disease in the elderly. Catarrhal conjunctivitis is caused by staphylococcal infection, often secondary to seborrhea. Gram-negative infections can be caused by chronic dacryocystitis or contaminated contact lenses. Adenoviral conjunctivitis, which is endemic and intermittently epidemic, is the most important viral infection. It is the most frequent cause of pink eye. HSV can cause kerato-conjunctivitis as well as herpes zoster. Both need to be ruled out before the patient is placed on any steroid containing medications.
Signs and Symptoms of Infectious Conjunctivitis
Bacterial Conjunctivitis Conjunctival edema Hyperemia Tearing Discharge (mucopurulent) Irritation Adenoviral Conjunctivitis Lymphadenopathy Hyperemia Lid edema Hemorrhage Corneal involvement Tearing
Herpetic Keratoconjunctivits Lymphadenopathy Hyperemia Lid edema Dendrites on the cornea (HSV more than Zoster) May have anterior segment inflammation
Signs and symptoms of infectious conjunctivitis depend on the causative agent. In patients with catarrhal conjunctivitis, for example, the conjunctiva becomes edematous and hyperemic. The papillary response gives it a velvety appearance. Tearing, mucopurulent discharge and irritation are the usual symptoms. In contrast, adenoviral conjunctivitis is characterized by a follicular reaction, lymphadenopathy. Corneal involvement is common and usually self limiting. Signs and symptoms include marked hyperemia, hemorrhages, lid edema and a watery, tear-like discharge. Herpetic keratoconjunctivits usually involves the corneal epithelium, with small corneal epithelial defects in a dendritic pattern. Often there is anterior segment inflammation. Zoster can occur along the 5th cranial nerve pattern and involve the eye. It is important to note that herpes infections need to be ruled out prior to stating any patient on any steroid or steroid-combination medication.
Treatment of Infectious Conjunctivitis
Bacterial or Catarrhal Conjunctivitis: Antibiotic A 4th generation fluoroquinone such as moxifloxacin (Vigamox) or gatifloxacin (Zymar) offers excellent broad spectrum coverage Dosage of tid-qid for 7 10 days Tears preparation, low viscosity, prn Cold compresses Viral Conjunctivitis: Prophylactic antibiotic bid x 5 7 days Tears preparation, low viscosity, prn Great care to not contaminate other members of the family Strict quarantine regarding shared washcloths, towels etc. Cold compresses
Treatment of infectious conjunctivitis depends on whether the infection is bacterial or viral in nature. Both can be symptomatically treated with a thin tear preparation and cold compresses. Patients with bacterial conjunctivitis should additionally receive antibiotics four times daily. Patients should also be warned that this disease is easily transmitted, especially viral pink eye conjunctivitis. Patients should be warned for strict quarantine of washcloths, towels, and frequent hand washing before dealing with others in the family.
Other Causes of Red Eye
Toxins (physostigmine) Reaction to topical medications Contact lens problems Pollution Alcohol Ultraviolet exposure Lack of sleep Allergies Foreign bodies Chemical burns Intraocular inflammation (uveitis)
Not every red eye is caused by infection. Conjunctival congestion can also be caused by air pollution, ultraviolet exposure, alcohol and lack of sleep. Allergic conjunctivitis, experienced by fifteen percent of the population, often results when an antigen, such as pollen, mediates a local immunoglobulin A or immunoglobulin E response. Use of topical medications or contact lens problems may also cause a red eye. A persistent achy red eye may signify uveal inflammation, and requires evaluation by an eye specialist.
Signs and Symptoms of Allergic Conjunctivitis
Itching Occasional burning Conjunctival injection, chemosis Watery or ropy discharge Lid swelling Redness Papillary response Possible eczema
Allergic conjunctivitis, more familiarly known as itchy eye, presents primarily as itching, with occasional burning. Conjunctival injection or chemosis will be seen, with a watery or ropy discharge and lid swelling. The characteristic redness maybe accompanied by an eczematous response. These patients frequently have other allergic symptoms such as allergic rhinitis.
Treatment of Allergic Conjunctivitis

Oral antihistamines (OTC) Thin tear preparation (OTC) Topical nonspecific antihistamine/vasoconstrictor drop (OTC): naphazoline (Vasocon, Naphcon) Specific antihistamine drop: Levocabastine (Livostin), an H1 blocker, 1 drop four times a day up to 2 weeks Mast cell stabilizer drop:4% cromolyn drops (Crolom) qid, nedocromil sodium (Alocril) or lodoxamide (Alomide), 1 2 drops four times a day Do not exceed 3 months use Olapatadine hydrochloride 1% (Patanol) drop :bid Epinastine HCl (Elestat) and ketotifen fumarate (Zaditor) Both have antihistamine and mast cell stabilizing actions Both are bid medications Ketorolac (Acular ), an NSAID drop, 1 drop four times a day for 7 days Or as a last resort: Mild topical steroids: Loteprednol etabonate (Alrex) or fluorometholone (last resort)
Allergic conjunctivitis can be treated with oral antihistamines. One drawback to the use of over-the-counter antihistamines is that they may exacerbate any underlying dry eye state. In addition, diphenhydramine may cause confusion in older patients and precipitate a cascade of adverse reactions with its use. Thin tear preparations such as HypoTears are useful in washing out the offending antigen. Other agents used to treat allergic conjunctivitis include nonspecific and specific antihistamines, mast cell stabilizers to inhibit the release of histamine, and non-steroidal anti-inflammatory drugs. Now, with Zaditor, Elestatand Patanolwe can combine H1 blockade with mast cell stabilization, and these drops are becoming the gold standard in treatment of allergic conjunctivitis. They provide immediate relief by blocking histamine receptors and also stabilize mast cells to prevent further immunoglobulin release. They are administered twice a day. Topical steroids are excellent treatments of allergic conjunctivitis, however, the long term use of steroids have multiple side effects such as cataracts, glaucoma, and thinning of conjunctival epithelium. They should not be the mainstay of treatment.
Etiology of Corneal and Uveal Tract Disease
CORENAL DISEASE Infection (H. simplex, zoster) Toxic reaction Metabolic changes Tear deficiency Trigeminal involvement Trauma Neoplasms
UVEITIS Infection (herpes, TB, etc.) Foreign bodies Systemic processes, such as rheumatologic disease Drug hypersensitivity Severe ischemia Surgical trauma Intraocular tumors
In addition to infections of the lid and conjunctiva, the elderly are at risk for infections of the cornea and uveal tract. Viruses and bacteria are leading causes of corneal disease. Infectious uveitis may be caused by systemic infection, herpes zoster ophthalmicus, herpes simplex virus, tuberculosis and other diseases.
Signs and Symptoms of Corneal Disease
Pain Photophobia Tearing Impaired vision Corneal immune precipitates Corneal edema Dendritic ulcers in the corneal epithelium (viral) Soupy ulcers (bacterial) Recurring lesions
The signs and symptoms of corneal disease are many and varied. Pain, caused by irritation of the ciliary nerves, is common, and often aggravated by light and pressure. Tearing is usually observed, secondary to reflex irritation of the cornea and ciliary nerves. Impaired vision may result from excessive light scatter, clouding of the stroma, epithelial edema, and scarring. Corneal disease may initially present as a superficial keratitis or a localized stromal edema, followed by the development of deep ulceration. Herpetic corneal disease may be recurrent, so inquiring about a history of prior lesions is important.
Signs and Symptoms of Uveitis
Pain Photophobia Tearing Impaired vision Corneal immune precipitates Corneal edema Bleeding into anterior chamber Vitreous opacities (posterior uveitis)
Although many of the signs and symptoms are similar to those of corneal disease, uveitis reflects a deeper intraocular process, secondary to either infection or other immune precipitated process. Protein and cells may coagulate on the cornea, lens, or on the vitreous.
Treatment of Corneal Infections

Bacterial Infections: Fluoroquinolones - e.g., Gatifloxacin (Zymar) and moxifloxacin (Vigamox) offer good broad spectrum coverage Fortified Antibiotics - e.g., cefazolin (Kefzol) 5% or tobramycin (Tobrex) 1.4% drops are made by injection of IV antibiotics into tear or standard preparations Viral Infections: Antiviral drops - e.g., trifluridine (Viroptic) 1% solution 1 drop in affected eye every 2 hours while awake, maximum 9 drops a day Decrease dose after epithelialization Do not use over 21 days Systemic antivirals - e.g., acyclovir (Zovirax) valacyclovir (Valtrex), famciclovir (Famvir) Fungal Infections: Antifungal medications (e.g., natamycin, Natacyn) 5% suspension 1 drop every 1-2 hours; after 3 to 4 days reduce to one drop 6 to 8 times a day Usual course of therapy is 2 to 3 weeks The treatment of corneal infection depends on the nature of the infection. In the past, bacterial ulcers were treated exclusively with pharmacist-prepared antibiotic eyedrops, such as fortified cefazolin or tobramycin. Today, fourth generations fluoroquinolones are frequently used instead. Antiviral therapy, such as trifluridine eyedrops, is used to treat herpes simplex virus or herpes zoster dendrite disease. Systemic antiviral agents are useful in treatment of herpetic infections when they include intraocular finding such as uveitis or active corneal dendrites. Antifungal medications such as natamycin are used to treat fungal ulcers.
Treatment of Uveitis
NSAID drops - e.g., diclofenac (Voltaren ), ketorolac (Acular ), flurbiprofen (Ocufen ) Topical steroid - e.g., prednisolone acetate (Pred Forte) 1%, dexamethasone (Ocu-Dex ) Rare: systemic immunosuppressant - e.g., oral prednisone, methotrexate
The mainstay of uveitis treatment is a strong anti-inflammatory eyedrop such as prednisolone acetate one percent. Subconjunctival injections of steroid prescribed by an eye specialist may supplement therapy. More rarely, oral prednisone or other systemic immunosuppressant such as methotrexate are used to treat uveitis in very refractive patients.
Resources
For additional information, see: Age related Eye Disease Study Research Group.A randomized, placebo-controlled, clinical trial of high dose supplementation with vitamins C and E, beta carotene and zinc for ARMD and vision loss.Report #8.Arch. Ophthalmol. 2001Oct;119(10):1417-36. Douglas, R., Jr., Cullom, B., & Chang.(1994). The Wills eye manual:Office and emergency room diagnosis and treatment of eye disease, 2nd ed.Philadelphia:Lippincott-Raven. Fechner, P. U. & Teichmann, K. D.(1998).Ocular therapeutics: Pharmacology and clinical application.Slack. Kertes, P.& Conway, M. D. (Eds.).Clinical trials in Ophthalmology:A summary and practice guide.William & Williams. MacCumber, M. W., (Ed.). (1997).Management of ocular injuries and emergencies. Philadelphia:Lippincott-Raven. American Academy of Ophthalmology, EyeNet http://www.eyenet.org/siteindex.html Karolinska Intitutet Library, Eye Diseases http://www.mic.ki.se/Diseases/c11.html
Glaucoma
By the end of this Review Concept you should be able to: Cite the epidemiologic trends associated with glaucoma. Differentiate between open angle glaucoma and angle closure glaucoma. Examine and apply patient, disease, and medication-related factors influencing the choice of treatment intervention for glaucoma. Describe the management of glaucoma-related adverse effects.
Incidence and Morbidity Associated with Glaucoma
Two million people afflicted annually in U.S. Five thousand people become legally blind each year Incidence increases with age 15% of adults > 80 years are affected With the aging of Americas baby boomers, one can expect the number of glaucoma patients to increase
Glaucoma afflicts over two million people in the United States, at least five thousand of which become legally blind as the disease progresses. Because the incidence of glaucoma increases with age, affecting over fifteen percent of patients eighty years and older, glaucoma is considered one of the most important geriatric disorders. As Americas population ages, we can expect a significant increase in the number of Americans with glaucoma.
Four Types of Glaucoma

Open angle glaucoma (OAG) (90% of all primary glaucoma cases) Angle closure glaucoma (ACG) (5% of all primary glaucoma cases) Combined mechanisms glaucoma Infantile glaucoma
Glaucoma is actually a group of diseases characterized by intraocular pressure too high for the optic nerve resulting in optic nerve atrophy and loss of visual field. At least four types of glaucoma are differentiated, based on alternative pathogenic mechanisms. A majority of glaucoma patients have high(greater that 21 mm mercury) eye pressures, though some patients with glaucoma progress with intracular pressures that were once consider safe.
Pathophysiology of Open Angle Glaucoma
Most open angle glaucoma occurs when the balance of aqueous humor production, and outflow through the eyes trabecular network becomes imbalanced. Despite a grossly open drain for aqueous outflow, higher intraocular pressure results, probably due to microscopic trabecular obstruction.
Risk factors for Open Angle Glaucoma
Family history Ethnicity (> in African Americans) Nearsightedness Diabetes Thyroid disease Steroids topical or systemic Thin corneas (less than 540 microns thick)
Risk factors for open angle glaucoma include family history, ethnicity, and thyroid disease. Six weeks of topical steroid treatment has been found to induce intraocular pressure spikes in five percent of normal patients and ninety-five percent of patients with existing open angle glaucoma. Family members, diabetics and nearsighted individuals are also at higher risk for intraocular pressure spikes with steroid use. Patients with chronic obstructive pulmonary disease or rheumatological problems should be monitored for open angle glaucoma. The newest risk factor for open angle glaucoma is a thin cornea. We are not sure if this risk factor is an independent factor or related to the fact that we can not accurately measure IOP in persons with thin corneas.
Diagnosis of Open Angle Glaucoma
Tonometry: Intraocular pressure (IOP) measurement (Schiotz, Goldman Applanation, Tonopen) Perimetry: Visual field examination (manual or automated) Gonioscopy: Eye drain inspection Optic nerve exam: To check degree of nerve atrophy Pachymetry: Corneal thickness measurement
Several tests aid in the diagnosis of open angle glaucoma. Tonometry measures intraocular pressure. Perimetry checks the visual field. Gonioscopy is usually performed to check the eyes ability to grossly drain aqueous humor. An optic nerve exam establishes the extent of neural axon loss due to optic nerve atrophy. Pachymetry measures the corneal thickness, alerting the physical if a cornea is abnormally thin as discussed in risk factors.
Clinical Features of Open Angle Glaucoma
Onset is gradual and asymptomatic Painless, usually elevated Intraocular pressure (IOP) i.e., >21mmHg White quiet eye Peripheral field defects, followed by eventual loss of central vision Grossly open drain Optic nerve with atrophy or cupping
Classic clinical findings in patients with open angle glaucoma include painless, elevated intraocular pressure, white quiet eye, and peripheral field defects. A grossly open drain may be seen and optic nerve atrophy or cupping.
Pathophysiology of Angle Closure Glaucoma
The clinical picture of angle closure glaucoma is distinctive from that of open angle glaucoma. In angle closure glaucoma, the iris is in opposition to the trabecular meshwork, blocking drainage of the aqueous humor. The result is acute or chronic increased intraocular pressure. In its chronic form, angle closure glaucoma presents much like open angle glaucoma, but with complete macroscopic drain closure.
Risk factors for Angle Closure Glaucoma
Farsightedness with crowded drainage angle Huge cataracts Ethnicity (> in Asians) Drugs Mydriatics, OTC vasoconstrictors, some cold medications., antihistamines
Risk factors for angle closure glaucoma include farsightedness and large cataracts. Asians seem to be more predisposed to this type of glaucoma. Drugs that can precipitate acute onset angle closure glaucoma include mydriatics, and on rare occasions, over-the-counter vasoconstrictors. Systemic atropine, cold medicines with pseudoephedrine, and antihistamines with cholinergic effects may also cause acute closure glaucoma in patients with anatomically predisposed eyes.
Clinical Features of Acute Angle Closure Glaucoma
Acute onset with HA, N/V, blurred or sudden loss of vision Red, painful eye with fixed mid-dilated pupil IOP extremely elevated Corneal edema, with halos around lights Closed drain
Clinical exam findings characteristic of acute angle closure glaucoma include acute onset with headache, nausea and vomiting, and blurred vision. Acute angle closure also manifests extremely elevated IOP, a red and painful eye, and a fixed mid-dilated pupil. Patients who present with this type of glaucoma require emergency treatment.
Pharmacokinetic Factors in Glaucoma Treatment

Conjunctival cul-de-sac holds only 7 l drop mixes with tears and most is lost through nasolacrimal duct Cornea absorbs medication, as long as medication is non-ionized or only partially ionized Intraocular absorption
Treatment of open angle or angle closure glaucoma is based on certain pharmacokinetic realities. The conjunctival cul-desac holds only about seven microliters of fluid, compared to thirty-nine microliters in an average drop. Much of the drop mixes with tears, and is lost through the nasolacrimal duct. The cornea absorbs medication, although its lipid-water composition inhibits passage of highly ionized drugs.
Treatment of Acute Angle Closure Glaucoma
Beta blocker Timolol (Timoptic ) 1drop, q20min x 2 Carbonic anhydrase inhibitor Acetazolamide (Diamox) po 2 x 250 mg, OR 1 2 drops of brizolamide (Azopt) or dorzolamide (Trusopt) Adrenergic stimulator Brimonidine (Alphagan) 1 2 drops Cholinergic stimulator Pilocarpine (Isopto Carpine, Pilocar) 1 drop of 2% every 5 minutes for 3 4 administrations, starting 20 minutes after the preceding medications have been applied Cover puncta during administration to decrease the possibility of systemic absorption Surgical procedures Often required to improve prognosis (e.g., Peripheral iridotomy) Also, an immediate paracentesis (incision into the eye to release fluid) if drops fail, often results in immediate resolution of the acute angle closure attack, allowing for iridectomy to be performed
Treatment of Acute Angle Closure Glaucoma

Acute angle closure glaucoma must be treated pharmacologically and surgically. Pharmacologic treatment of emergent angle closure glaucoma relies initially on the use of beta blockers, alpha agonists, and carbonic anhydrase inhibitors which reduce aqueous humor formation. The beta blocker timolol comes in a gel forming solution and offers up to fifty times greater corneal contact time than comparable drugs. Two-two hundred fifty milligram tablets of the carbonic enzyme inhibitor, acetazolamide, may also be administered, or alternatively, 1-2 drops of a topical carbonic anhydrase inhibitor, such as brinzolamide or dorzolamide can be applied. Brimonidine is given to relieve intraocular pressure. Pharmacologic treatment of acute angle closure glaucoma also includes the use of the cholinergic stimulator, pilocarpine, which constricts the pupil and pulls the iris out of the drain. If a patient has medical contraindications to pharmacologic treatment by beta blockers (i.e. asthma) or carbonic anhydrase inhibitors (i.e. sulfur allergy), a paracentesis may be performed to break the acute angle closure attack. Either way, once the acute attack is ended, a peripheral iridectomy must then be scheduled.
Treatment of Chronic Angle Closure Glaucoma

Timolol (Timoptic) Dosage:qd bid ADRs:Ocular or corneal irritation, arrhythmia, bronchospasm, depression, fatigue Brimonidine (Alphagan) or Dorzolamide (Trusopt) Dosage:bid ADRs:Allergy, reactive hyperemia, mild mydriasis, macula edema with decreased vision, adrenochrome deposits sleepiness Brinzolamide (Azopt) or Dorzolamide(Trusopt) Dosage:bid ADRs:Allergy, mild hyperemia, bad taste in mouth Pilocarpine (Isopto Carpine, Pilocar) Dosage:qid ADRs: Ciliary muscle spasm, browache, miosis, increased risk of cataracts, retinal detachment, diaphoresis, diarrhea, increased cognitive dysfunction, decreased RBC, pseudocholinesterase Latanoprost (Xalatan),Travoprost (Travatan), or Bimatoprost (Lumigan) Prostaglandin analogs Dosage:qHS ADRs:Hyperemia, iritis macula edema, trichiasis
Treatment of Chronic Angle Closure Glaucoma
Chronic angle closure glaucoma may be treated pharmacologically or surgically. Again, beta blockers, alpha agonists, topical carbonic anhydrase inhibitors, and cholinergic stimulators are key to successful treatment, although long term use of these medications is not without side effects. Timolol can produce occasional ocular burning or corneal irritation, possible arrhythmia or bronchospasm, and changes in mental state. Pilocarpine is known to produce retinal detachment, diarrhea, and cognitive dysfunction. Dorzolamide or brinzolamide may be prescribed as an alternative to timolol or pilocarpine. Topical CAIs have almost completely replaced the systemic variety (acetazolamide) for chronic therapy since it has fewer side effects. Side effects of topical CAIs include allergy, red eye, and bad taste in the mouth. Brimonidine also may be associated with a red eye, and can cause drowsiness in the elderly. Finally, the newest class of glaucoma medications, prostaglandin analogs, are increasingly used in this group of patients with excellent success.
Treatment of Chronic Open Angle Glaucoma

Beta blocker qd, if no contraindications Brimonidine (Alphagan) bid tid Dorzolamide (Trusopt), brinzolamide (Azopt) bid tid Latanoprost (Xalatan), Travoprost (Travatan), or Brimonidine (Lumigan) qHS Laser Trabeculoplasty Filter surgery
Treatment of chronic open angle glaucoma may also be pharmacological or surgical. A beta blocker one to two times a day may be prescribed if there is no contraindication. Brimonidine, brinzolamide, or dorzolamide may also be used bid-tid. The prostaglandin analogs, latanoprost (Xalatan), travoprost (Travatan) and bimatoprost (Lumigan) are excellent as first line therapy. Side effects are usually mild, such as hyperemia, or hypertrichiasis, but may include more severe intraocular side effects such as macular edema. In fact, extreme side effects of long-term use have led to decreased use of Pilocarpine, apraclonidine, dipivefrin (Propine), acetazolamide (Diamox), methazolamide (Neptazane) and epinephrine to treat chronic open angle glaucoma. If medications and/or laser trabeculoplasty are not able to control the intraocular pressure, then filter surgery may be recommended to make a new drain for the affected eye.
Differential Diagnosis of Red Eye in Patients with Glaucoma

Infection or filtering bleb Allergy to topical glaucoma medications Dry eye due to long standing use of medications Non-allergic chemical reaction to medications
Patients who have been treated for glaucoma for a period of time may develop red eye for a variety of reasons. They may, for example, have an infection of a previous filtering bleb, producing blebitis or endophthalmitis. They could be experiencing an allergic or non-allergic reaction to glaucoma medication(s), which is common with the use of alpha agonists and topical carbonic anhydrase inhibitors. In fact, all the prostaglandin analogs may cause a red eye for the first 2-3 weeks, which usually resolves. A differential diagnosis is important in determining the best way to relieve the discomfort associated with glaucoma-related red eye.
Infection of a Filtering Bleb

Bleb: An irregularly shaped elevation of the conjunctiva, which normally appears clear, but may, when infected, contain pus and appear translucent or opaque
If a patient has a red eye and a history of glaucoma surgery (trabeculectomy), one of the first diagnoses that need to be ruled out is an infected. An infected bleb will appear as white or opaque, often with purulent discharge. Cultures of the eyelid and conjunctiva may help identify the bacteria involved. Because of the risks associated with unchecked infection, glaucoma patients who present with red eye and a filtration bleb need to be examined by an ophthalmologist as soon as possible. This is an ocular emergency and the patient should be instructed to go the Emergency room if after hours.
Treatment of Infected Bleb or Eye

Blebitis: 1-2 drops of 2 topical antibiotics q30 minutes around the clock Cefazolin Tobramycin Vancomycin Ofloxacin or ciprofloxacin (Ciloxan) Endophthalmitis: Intraocular injection, variably, of: Gentamicin 100 mcg in 0.1 cc Vancomycin 1 mg in 0.1 cc Clindamycin 450 mcg in 0.1 cc Cefazolin 2.25 mg in 0.1 cc Amikacin 400 mcg in 0.1 cc Ceftazidime 2.25 mg in 0.1 cc
If the patient is diagnosed with blebitis, and the infection is confined to the bleb itself, initial treatment is based on extensive use of topical antibiotics such as cefazolin, tobramycin, vancomycin or a fluoroquinolone. If the diagnosis points to endophthalmitis, where both the anterior segment and vitreous are involved, then initial treatment consists of injection of intravitreal antibiotics. When cultures point to a specific pathogen, additional antibiotic treatment is tailored accordingly.
Allergic Reaction to Glaucoma Medication

MEDICATION Timolol Dorzolamide Brimonidine Pilocarpine Apraclonidine Dipivefrin Latanoprost Travoprost Bimatoprost PROBABLITY OF ALLERGIC REACTION Unlikely 10 20% 10 15% 5% Approaches 50% Approaches 50% 3 5% 3 5% 5%
Once blebitis and endophthalmitis have been ruled out, reactions to glaucoma medications must be considered. Glaucoma patients that present with not only red eye, but also with lower eyelids that are red and swollen, suggest the presence of an allergic drug reaction to either the preservatives in the medication or the medication itself. If the patient already had dry eye, the reaction may be exacerbated. Treatment focuses on stopping the offending agent and moving on to some other therapy.
Chemical Irritation Cause by Glaucoma Medications

Frequently associated with the first several weeks of prostaglandin analog therapy Discontinue suspected medication(s) only if redness continues after 2 3 weeks Prescribe preservative-free, artificial tears Monitor IOP without glaucoma drops
Red eye may also be the result of chemical irritation rather than an allergic reaction; we see this during the first 2-3 weeks of initial prostaglandin analog use. Fortunately, it usually self resolves. If it does not, then the suspected medication or medications must be stopped immediately. Preservative-free artificial tears may be prescribed to relieve discomfort.Steroid drops can usually be avoided.
When Pharmaceutical Treatment Fails
Various surgical options should be considered: Laser trabeculoplasty with open angle glaucoma Trabeculectomy Glaucoma drainage device
Many cases of advanced glaucoma cannot be controlled by topical medications alone. In cases where progressive optic nerve atrophy continues to occur despite maximum tolerated medicine therapy, then surgical options should be considered. Surgical options for open angle glaucoma patients include laser trabeculoplasty in open angle glaucoma, and for all types of glaucoma, trabeculectomy and glaucoma drainage device surgery.
Laser Trabeculoplasty
Uses a laser to treat the eyes natural drain so that it drains more efficiently Argon laser trabeculoplasty (since 1980), not repeatable Selective laser trabeculoplasty (since 2001), is repeatable Success rates of laser trabeculoplasty range from 66%-90% depending on the type of glaucoma and the nature of the drain
If an open angle glaucoma patient is not controlled on medications, the next step considered by the ophthalmologist is laser trabeculoplasty. This procedure is done in the office and works by applying just enough energy to the surface of the eyes drain that it opens up more on a microscopic level. Both argon and the newer Selecta (YAG laser) are used for this surgery. The success rate for laser trabeculoplasty ranges from 66-90%.
Trabeculectomy Surgery, (a.k.a. filter surgery)
Incisional surgery in the operating room Makes a new drain hole for the eyes fluid to filter out of the eye Results in a bleb, i.e.:collection of eye fluid (aqueous) in the subconjucntival space
If laser trabeculoplasty fails in the open angle glaucoma patient, of if a closed angle patient needs additional treatment beyond the initial laser iridectomy and subsequent medicine treatment, then trabeculectomy surgery is performed. The patient is treated in the operating room where the surgeon makes a new drain hole for the eyes fluid to drain out, thus reducing the eyes pressure.
Repeat Warning
If a patient presents with a red eye, they need to be asked if they have a history of glaucoma surgery The new drain facilitates entry of bacterial into the eye, risking endophthalmitis (infection inside the eye) If the answer is yes, then refer the patient emergently to the eye doctor
It cannot be emphasized enough, that a red eye in a patient with an existing trabeculectomy can be associated with progression to blindness due to infection, if appropriate treatment is not immediately instituted.
Glaucoma Drainage Device Surgery
An alternative glaucoma incisional surgery is glaucoma drainage device surgery A hollow 22 gauge tube is placed inside of the eye Fluid drains through this tube to a plate sutured in the subconjunctival space in the back of the eye
Not all eyes are trabeculectomy candidates (patients with uveitic glaucoma, or juvenile glaucoma); other eyes progressive glaucoma fail trabeculectomy surgery (the new drain heals up).In these cases, the next step usually involves insertion of a hollow drainage tube into the eye, a glaucoma drainage device.
Different Glaucoma Drainage Devices

Baerveldt tubes Ahmed tubes Molteno tubes Krupin tubes
Multiple different drainage devices are available to help drain fluid out of the eye, and lower the intraocular pressure. They all work similarly.
Post-Op Glaucoma Surgery Patients

Any patient in the postoperative period following glaucoma surgery: Should be encouraged to use their prescribed topical medications: 1. Usually a topical antibiotic 2. A topical steroid 3. Occasionally a topical cycloplegic They should call their surgeon if any change in vision occurs, if redness develops, or if pain or discharge develops
The pharmacist should be aware that the success of almost all glaucoma surgery is dependent on proper application of postoperative topical prescribed eyedrops. Also, should a patient develop a postoperative problem, such as a drop in vision, red eye, pain, or discharge, they should call their surgeon immediately
Resources
For additional information, see: Kertes, P.& Conway, M. D. (Eds.).Clinical trials in Ophthalmology: A summary and practice guide.Baltimore:William & Williams. Kunimoto, D, et al. (2002) The Wills eye manual:Office and emergency room diagnosis and treatment of eye disease, 3rd ed.Philadelphia:Lippincott-Raven. Lichter PR (2003).Glaucoma clinical trials and what they mean for our patients.Am J Ophthalmol 136: 136-145. Rhee, D & Deramo V (2001)Wills Eye Drug Guide2nd Edition.Lippincott, Williams, and Wilkins Shields, B. (1998).Textbook of glaucoma. Baltimore: William & Wilkins. American Academy of Ophthalmology, EyeNet Karolinska Intitutet Library, Eye Diseases New York University Department of Ophthalmology, Digital Ophthalmic Slide Collection

Module 15 - Pharmacotherapy For Ophthalmological Disorders

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Geriatric

Pharmacy Review Module 15 Pharmacotherapy for Ophthalmological Disorders

Copyright 2011 American Society of Consultant Pharmacists

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Degenerative Diseases of the Elderly Eye

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Age-related Changes in the Eye

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Age-related Changes in the Eye

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Signs and Symptoms of Dry Eye Syndrome

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Risk Factors for Dry Eye Syndrome

Treatment of Dry Eye Syndrome

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Degenerative Diseases of the Lens and Retina

Diseases of the Lens Cataracts

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Effects of Cataracts on Vision

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Steps in Cataract Extraction (Phacoemulsification)

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Pre-operative Preparation for Cataract Extraction

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Post-operative Management for Cataract Extraction Topical Antibiotics

Monitor for: Development of antibiotic toxicity

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Post-operative Management for Cataract Extraction Anti-inflammatory Drugs

as 1 week after initiation

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Post-operative Red Eye

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Incidence of Macular Degeneration

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Pathogenesis of Macular Degeneration

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Clinical Signs of Macular Degeneration

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Management and Treatment of Macular Degeneration

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Diseases That Affect the Eye: Diabetes

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Diseases That Affect the Eye: Hypertension

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Common Infections of the Eye

DISORDER Blepharitis Conjunctivitis Corneal disease / ulcers Cellulitis Uveitis Lids

Conjunctiva Cornea Orbits Uveal tract

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Etiology and Pathogenesis of Blepharitis

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Clinical Signs and Symptoms of Blepharitis

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Common Conjunctival Infections and Their Causes

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Signs and Symptoms of Infectious Conjunctivitis

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Treatment of Infectious Conjunctivitis

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Other Causes of Red Eye

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