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SIGNS AND SYMPTOMS
Patients may present with blurred vision, pain, photophobia and tearing following blunt, concussive injury to the eye or orbit. Hyphemas (blood in the anterior chamber) are described by the amount of anterior chamber (AC) they occupy: Grade 1 = less than one-quarter of the visible volume of the AC Grade 2 = one-quarter to one-half of the visible volume of the AC Grade 3 = one-half to three-quarters of the visible volume of the AC Grade 4 = complete filling of the visible AC The term "eight-ball hemorrhage" is reserved for completely filled anterior chambers with black-colored clots.
There are two suggested mechanisms of hyphema formation. Either direct, contusive forces cause mechanical tearing of the fragile blood vasculature of the iris and/or angle, or concussive trauma creates rapidly rising intravascular pressure within these vessels, resulting in rupture. Blood in the AC is not by itself necessarily harmful. However if quantities are sufficient it may obstruct the outflow of aqueous humor, resulting in glaucoma. Hemolytic glaucoma results from direct obstruction of the trabecular meshwork by fresh blood. Hemosiderosic glaucoma results from trabecular meshwork obstruction from degrading hemoglobin. Ghost cell glaucoma results from trabecular meshwork obstruction by the skeletons of the disintegrating red blood cells. Finally, any external force strong enough to produce internal bleeding is also sufficiently strong to produce direct damage to the adjacent trabecular meshwork, resulting in sluggish aqueous drainage (late glaucoma).
A thorough history is critical. Circumstances surrounding the event, current medicines and previous ocular history are important pieces of data. Bleeding in the eye warrants questioning concerning systemic blood disorders such as sickle cell anemia, hemophilia and Von Willebrand's disease (vascular hemophilia). If the patient is a poor historian or questions arise regarding systemic health, order systemic tests for sickle cell anemia (sickle prep or sickle dex) and bleeding disorders (PT and PTT). Ocular examination should include an evaluation of the adnexa (X-ray, CT scan to rule out fracture or entrapment) cornea (to rule out perforation), sclera (to rule out ruptured globe), anterior chamber, lens, vitreous and retina. If a clear view of the fundus is obstructed by the hyphema or vitreous hemorrhage, perform or refer for a B-scan ultrasound of the globe. Whether these individuals should be hospitalized is controversial. Most practitioners manage uncomplicated hyphemas (grade 1) without hospital admission. Cycloplege the patient with atropine 1% BID/QID and prescribe a steroid such as Pred Forte or Vexol Q2H/QID. If intraocular pressure is above 27mm Hg, it should be controlled using topical beta-blockers BID. When IOP requires acute attention (i.e., over 35mm Hg) prescribe acetazolamide 500mg PO BID, barring systemic contraindications, until the pressure is adequately controlled. If there are corneal epithelial defects, Rx a topical antibiotic prophylactically. Instruct the patient to limit activity to the bathroom and bed rest, laying with the head elevated at an angle of 30 degrees. Provide an eye shield for additional protection. To prevent re-bleeding, use only acetaminophen to manage pain; avoid aspirin and ibuprofen. Referral for surgical evaluation is indicated if there is corneal blood staining, if IOP is greater than 60mm Hg, if there is
an eight-ball hemorrhage or if the IOP remains above 35 for seven days. Follow up with VA, slit lamp, IOP and dilated fundus exam for four consecutive days, then as necessary.
Gonioscopy is contraindicated because it increases the risk of re-bleeding. However, up to 50 percent of patients with hyphema possess angle recession and the possibility of developing a secondary traumatic late glaucoma. Monitor the IOP of these patients regularly. The onset of secondary glaucoma is between 12 months and 50 years. Perform gonioscopy after the event has resolved and the risk of re-bleeding has passed. • Aminocaproic acid (Amicar 50mg/kg), an antifibrinolytic, has been advocated by some to reduce the risk of re-bleeding. One of its potential side effects is severe nausea and vomiting, a contraindication in patients with hyphema. The medicine seems to function best in children but is not universally accepted and remains controversial.
PRIMARY OPEN ANGLE GLAUCOMA (POAG)
SIGNS AND SYMPTOMS
Although early POAG patients are virtually asymptomatic, there are at least three definitive signs: elevated intraocular pressure (approximately 21mm Hg or more), enlargement of the optic cup and repeatable field loss. Other possible signs include nerve fiber layer dropout, notching of the neuroretinal rim at the inferior or superior poles, and splinter hemorrhages adjacent to the optic disc.
Despite decades of research and over two million diagnosed cases of open angle glaucoma in the U.S. alone, much remains unknown about this disease. Elevated intraocular pressure almost certainly plays a significant role, but the process is poorly understood. According to the mechanical theory of POAG, chronically elevated IOP crimps the axons of retinal ganglion cells as they pass through the lamina cribrosa, eventually killing the cells. The vascular theory suggests that, with elevated IOP, reduced blood flow to the optic nerve starves the cells of oxygen and nutrients. New research presented in 1996 offers another possible mechanism of ganglion cell death. Studies show that some glaucoma patients exhibit elevated levels of the neurotransmitter glutamate within the vitreous. Ganglion cells contain protein receptors that, when activated by glutamate, increase intracellular calcium to toxic levels, killing the cells.
Although several new IOP lowering drugs have been released in the past few years, beta-blockers continue to be the mainstay of glaucoma therapy. The typical management plan is to set a target IOP at least 25 percent below pre-treatment levels, and prescribe your beta-blocker of choice two or three times per day until the target is reached. The 19-year-old timolol (Timoptic) is the most commonly prescribed beta-blocker available, but others are also noteworthy. Betimol from Ciba Vision Ophthalmics is a new, low-cost formulation of timolol that, unlike Timoptic, cannot be surreptitiously replaced with a generic by the pharmacist. A familiar but often overlooked beta-blocker that is gaining in prominence is betaxolol (Betoptic). This drug selectively blocks beta-1 receptors, largely sparing beta-2 receptors in the lungs and thereby making it
a safer option for patients with some pulmonary conditions. Betoptic also has less likelihood of reducing blood flow (and may, in fact, increase perfusion) to the optic nerve than other beta-blockers, has less propensity to reduce the levels of HDL cholesterol in blood, and preserves the visual field equally or better than other beta-blockers, even though its IOP reduction tends to be somewhat less. Finally, new research also shows that betaxolol provides ganglion cells with at least some protection from calcium toxicity caused by glutamate binding. Other unique beta-blockers include carteolol, which, like betaxolol, has less propensity to reduce HDL cholesterol levels, and Timoptic-XE, which allows for once-a-day therapy. New medications such as the prostaglandin analog latanoprost (Xalatan) and the topical carbonic anhydrase inhibitor dorzolamide (Trusopt) offer alternative therapies, but beta-blockers have been the gold standard against which all new pressure lowering medications are measured, and this is unlikely to change. In all likelihood, beta-blockers will remain the first-line therapy of choice in POAG, and prostaglandin analogs will supplant older second-line therapies. Xalatan is comparable in IOP lowering effect to Timoptic; its main side effect is darkening of the pigment in light-colored irises. Another new IOP lowering drug, the alpha-2 adrenergic agonist brimonidine (Alphagan), has not been proven clinically superior to apraclonidine (Iopidine) although it is approved for chronic use whereas Iopidine 1% is intended to control post-surgical pressure spikes and angle closure attacks. A lower concentration, Iopidine 0.5%, has been developed and approved for chronic care of POAG patients. It is likely that Alphagan and Iopidine will equally share the alpha-2 adrenergic agonist market.
Prostaglandin analogs reduce IOP by increasing aqueous outflow through the uveoscleral pathway by dilating the spaces between ciliary muscle bundles. However, miotics such as pilocarpine tighten these bundles by contracting the iris dilator muscle, so these two medications are counter-effective. Discontinue any miotics prior to adding Xalatan to the regimen. To improve compliance for patients on multiple medications, it is helpful to identify the cap colors of each drug being used (e.g., "Remember to use the one with the yellow cap twice a day and the blue one four times a day.")
ACUTE ANGLE CLOSURE GLAUCOMA
SIGNS AND SYMPTOMS
Patients with angle closure glaucoma manifest symptoms of ocular and facial pain, unilateral blurring of vision, photopsiae in the form of colored haloes around lights, and occasionally nausea and vomiting. Acuity may be reduced significantly in the involved eye, often to 20/80 or worse. The hallmark signs of angle closure include significantly elevated intraocular pressure, a closed angle upon gonioscopic evaluation, deep conjunctival and episcleral injection in a circumlimbal fashion, and a fixed, mid-dilated pupil. Upon slit-lamp examination, you may also see an edematous or "steamy" cornea and shallow anterior chamber. Applanation tonometry may reveal IOP in the range of 30 to 60mm Hg, or even higher in some cases. Gonioscopy, which may prove difficult because of microcystic corneal edema, reveals no visible angle structures without indentation. There may be evidence of previous angle closure episodes in the form of peripheral anterior synechiae (PAS) in the fellow eye.
Angle closure occurs when the peripheral iris physically opposes the trabecular meshwork or corneal
Once you have established angle closure as the cause. anterior uveal displacement (such as in choroidal detachment) or.5% BID. prednisolone acetate 1% QID. Once the IOP is below 40mm Hg. or from posterior synechiae. as this will only exacerbate the condition. whereby the flow of aqueous from the posterior to anterior chamber is inhibited. administer an oral carbonic anhydrase inhibitor (acetazolamide 2 x 250mg tablets)." Patients with this presentation may boast a deep anterior chamber centrally. The most common etiology of angle closure is pupillary block. and oral acetazolamide 500mg BID. immediately treat such patients with a beta-blocker of 0.5% concentration and/or apraclonidine 1%. the iris demonstrates an unusual laxity. It may be necessary to use topical glycerin to clear the cornea if there is significant edema. You may also wish to use a hyperosmotic agent such as three to five ounces of oral glycerin or isosorbide over ice. rarely. you must also differentiate the nature of the attack. Next. Your choice of primary medication depends upon the pressure at presentation. glaucomatocyclitic crisis and phacolytic glaucoma. perform corneal compression with a gonioprism to aid in lowering the IOP by forcing aqueous into the trabeculum and temporarily opening the angle. If the patient does not achieve significant reduction in IOP after 45 minutes. refer the patient for a peripheral iridotomy. causing iris bombé. instill pilocarpine 2% as well as prednisolone acetate 1% every 15 minutes to abate the attack and reopen the angle.endothelium and impedes aqueous outflow. It is safe to discontinue this regimen when the IOP is below 30mm Hg and the angle structures are again visible with gonioscopy. lenticular enlargement or displacement of the lens or IOL (secondary pupil block). When the inflammation has diminished and the AC is quiet. This may be simply due to genetic predisposition and anterior segment anatomy (primary pupil block). If you are uncertain of the etiology or if an inflammatory glaucoma is present. First distinguish between angle closure glaucoma and other acute open angle conditions such as uveitic glaucoma. Perform tonometry every 15 minutes after initiating therapy. plateau iris. whether due to primary pupillary block. the socalled "plateau iris syndrome. Several mechanisms are possible. CLINICAL PEARLS • The most important consideration in handling an acute angle closure attack is accurate diagnosis and prompt intervention. do not use a miotic. This provides a secondary outflow channel for aqueous. These patients may be prone to "angle crowding" and subsequent closure during physiologic or pharmacologic dilation. however. Another mechanism which may induce angle closure involves an abnormal configuration of the iris. and commonly causes a permanent anatomical "deepening" of the anterior chamber. Other etiologies of angle closure without pupil block include neovascular membranes inducing PAS. coming into close approximation with the angle peripherally. ANTERIOR UVEITIS . posterior segment inflammation or tumors. timolol (or equivalent) 0. or secondary pupillary block. MANAGEMENT The paramount concern in managing an angle closure attack is to lower IOP quickly. Maintain the patient on the following medications: pilocarpine 2% QID. As most miotics are ineffective at pressures over 40mm Hg due to iris ischemia.
quell the inflammatory response. Associated sensitivity to lights may be severe. depending upon the severity of the reaction. However. syphilis. often. although the palpebral conjunctiva is characteristically normal. inflammatory reactions in adjacent tissues (e. PATHOPHYSIOLOGY Uveitis. In more severe reactions. resulting in a secondary uveitic glaucoma. Inspection may reveal mild to moderate congestion of the lids. First. although patients may report some haziness. Treat secondary elevations in IOP using standard anti-glaucoma agents. Behçet's syndrome. ankylosing spondylitis. After beginning treatment. appearance. these patients will present wearing dark sunglasses. however. you may observe grayish brown endothelial deposits. and patients may need to remain on steroid drops daily or every other day for several weeks. The cornea may display mild edema upon biomicroscopy. less commonly. If this debris builds significantly. Uveitis can be either acute or chronic. The chronic form is more often associated with systemic disorders including. You'll typically see a deep perilimbal injection of the conjunctiva and episclera. Inflammation may be associated with underlying systemic disease. and is not associated with a foreign body sensation. Chronic uveitis most likely occurs due to an immunopathological mechanism which is not fully understood. flare refers to liberated protein from the inflamed iris or ciliary body which gives the aqueous a particulate. Reiter's syndrome. you may see granulomatous nodules within the iris stroma.. prescribe a topical steroid Q2-3H. as the name implies. Second. dull aching of the involved eye and surrounding orbit. Next. or more often if the reaction is severe. discontinue the cycloplegics and taper the steroids to QID or TID. such as timolol 0." Cells are leukocytes (white blood cells) floating in the convection currents of the aqueous. keratitis). In recalcitrant uveitis which is unresponsive to conventional therapy. The excessive tearing occurs secondary to increased neural stimulation of the lacrimal gland. scopolamine 0. inflammatory bowel disease. Intraocular pressure in the affected eye is initially reduced due to secretory hypotony of the ciliary body. If there's a posterior synechia present. or smoky. Occasionally. known as keratic precipitates. tuberculosis. sarcoidosis.5% BID or dorzolamide 2% TID. the pressure may rise sharply. to the peripheral cornea (anterior synechia). Additionally. immobilize the iris and ciliary body to decrease pain and prevent exacerbation of the condition. as the reaction persists. Begin by cyclopleging the patient with homatropine 5% TID/QID. juvenile rheumatoid arthritis. as it will only serve to worsen the inflammatory response by mobilizing the uveal tissues. re-evaluate the patient every one to seven days depending on the severity of the reaction. but not limited to.SIGNS AND SYMPTOMS The typical presentation of anterior uveitis involves pain. resulting in pseudoptosis. inflammatory by-products may accumulate in the trabeculum. and if the ciliary body resumes its normal secretory output. Patients report a deep. MANAGEMENT There are two primary goals when managing anterior uveitis. may prove more difficult and uncomfortable. The iris may adhere to the lens capsule (posterior synechia) or. photophobia and excessive tearing. can induce a secondary uveitis. Visual acuity is not usually impaired to any great extent (20/40 or better is common). consider injectible steroids such as methylprednisolone 60mg or even oral steroids such as prednisone 60 to 80mg. represents an inflammation of the uveal tissues. Generally. attempt to break the adhesion in the office using atropine 1% and phenylephrine 10%. . The hallmark signs of anterior uveitis are "cells and flare.g. it is better to taper slowly rather than abruptly. chiefly the iris and ciliary body. or it may occur as a direct result of ocular trauma. Accommodative tasks.25% BID/QID or atropine 1% BID. Avoid pilocarpine in uveitic glaucoma. As the uveitis resolves. and Lyme disease.
This mechanism is similar to the previous two types of glaucoma. HLA-B27.CLINICAL PEARLS • • Acute anterior uveitis results most commonly as a result of blunt ocular trauma. Consider any cases of recurrent uveitis. the glaucoma is typically very symptomatic with pain and redness in the involved eye. fluorescent treponemal antibody absorption (FTA-ABS) and rapid plasma reagin (RPR). The angle remains open. with a history of cataracts. • LENS INDUCED GLAUCOMAS SIGNS AND SYMPTOMS The lens induced glaucoma patient is typically elderly. In most instances. and attenuation of the capsule with the release of lens proteins into the anterior chamber. PATHOPHYSIOLOGY Phacolytic glaucoma This condition involves a hypermature cataract with severe visual reduction (typically light perception). rheumatoid factor (RF). Anterior uveitis may actually constitute a "spillover" of posterior ocular inflammation. . except that inflammatory cells are not limited to macrophages. become bloated. and cells and flare in the anterior chamber. defined as three or more unexplained incidents. A chest X-ray is also important in identifying both sarcoidosis and tuberculosis. There are four types of glaucomas associated with lens complications (excluding cases of lens displacement in ectopia lentis): • • • • phacolytic glaucoma lens particle glaucoma phacoanaphylactic uveitis phacomorphic glaucoma In all of these cases. and block trabecular outflow. The angle may be open or closed. these cases resolve without incident and do not recur when properly managed. though in some cases peripheral anterior synechiae may develop. Frequently. Always perform a comprehensive. to be representative of underlying systemic inflammatory disease until proven otherwise. It's characterized by acute onset of pain and redness and IOPs often of 35mm Hg or greater. Also. chronic or bilateral presentation. except that there is a history of surgery or trauma that releases the lens proteins into the anterior chamber and initiates a macrophage-driven inflammatory reaction. The angle remains open. an advanced cataract in the involved eye severely reduces vision. Lens particle glaucoma The mechanism of lens particle glaucoma resembles that of phacolytic glaucoma. there is considerable flare and mutton-fat keratic precipitates. There is liquefaction of the lens nucleus and cortex. A standard battery of laboratory tests should include: complete blood count (CBC) with differential. dilated fundus evaluation in these cases. purified protein derivative (PPD). A Lyme titer is also recommended if you suspect that the patient may have been bitten by a deer tick. and a propensity for synechiae formation. Phacoanaphylactic uveitis This is a chronic uveitis that occurs one to 14 days following cataract extraction or lens trauma. angiotensin-converting enzyme (ACE). Hematologic testing is indicated for any recurrent. antinuclear antibody (ANA). Macrophages engulf the lens proteins.
consider phacomorphic glaucoma. CLINICAL PEARLS • • • • In cases of severe granulomatous uveitis with IOP rise following cataract extraction. PATHOPHYSIOLOGY Due to accumulation of abnormal basement membrane material at the pupillary margin. some have observed exfoliative material deposits on intraocular lens implants. this coalesces into a characteristic "bulls-eye" pattern seen in pseudoexfoliation. In cases where the lens precipitates a secondary glaucoma. the best management is surgical lens removal.Phacomorphic glaucoma In this case. Avoid miotics and prostaglandin analogs in cases where inflammation is present. the cataract reduces vision severely. There is no racial. In cases where there is phacomorphic glaucoma in a nanophthalmic eye. there may be observable pigment or clear flaky material. surgical excision of the cataract is associated with severe complications of choroidal detachment and hemorrhage. Phacomorphic and phacolytic glaucoma develop only in eyes with hypermature cataracts. Vision typically ranges from 20/400 to light perception. Typically. PSEUDOEXFOLIATION SYNDROME AND PSEUDOEXFOLIATIVE GLAUCOMA SIGNS AND SYMPTOMS Patients with pseudoexfoliation syndrome remain asymptomatic until an advanced glaucoma develops. you may prefer medical therapy and laser iridotomy rather than surgical management. The condition is most common in the sixth to eighth decade. In patients with hypermature cataracts and shallow anterior chambers with angle closure. The angle in this glaucoma is closed. and not flaking-off of the lens capsule. This leads to increased iris transillumination and deposition of pigment granules on the endothelium. There is often increased transillumination of the iris at the pupillary margin and there may be pigment granules on the endothelium and iris surface. The patient presents with a fine. In cases where there is significant anterior segment inflammation. elevated IOP develops in up to 80 percent of patients. an increase of lens thickness from an advancing cataract leads to a relative pupil block. intraocular pressure is unaffected. there is increased apposition with the iris and subsequent erosion of iris pigment as the pupil dilates and constricts. glaucomatous cupping and visual field loss may ensue. especially if the fellow lens has less intumescence and there is a deeper chamber. carbonic anhydrase inhibitors and alpha adrenergic agonists to temporize the IOP. lensectomy is not a remedy. consider phacoanaphylactic uveitis. use topical steroids to quell the inflammation. MANAGEMENT Employ topical beta blockers. The intumescence often develops quickly. with actual glaucoma developing later in this age range. Because this condition involves deposition of material on the anterior lens capsule. Within the angle. . In fact. but becomes bilateral within about seven years. flaky material on the anterior lens capsule at the pupillary margin. If vision is better than 20/400. pseudoexfoliation syndrome begins unilaterally. Typically. posterior bombé and angle closure. Initially. sexual or geographic predilection. In these cases. however. iris surface and trabecular meshwork similar to pigment dispersion syndrome. consider another cause for the glaucoma. In these cases. Over time.
studies have identified patients with increased IOP but no decrease in aqueous outflow. diabetic retinopathy. However. NVG typically develops within three . Funduscopically. painful eye which often has significant vision loss. there will be total or near-total angle closure. prostaglandin analogs and alpha adrenergic agonists if not systemically contraindicated. Pathophysiology Ischemia to ocular tissues is theorized to be the genesis of NVG. and carotid artery disease and ocular ischemic syndrome (OIS). or giant cell arteritis (GCA). CLINICAL PEARLS • An initially normal IOP measurement does not preclude prior IOP elevation with subsequent field loss and disc damage. the IOP level in pseudoexfoliative glaucoma is typically higher than in POAG and is more difficult to temporize. MANAGEMENT Pseudoexfoliation syndrome without a pressure rise requires only periodic monitoring of IOPs. discs and visual fields. carotid artery disease. there will be significant concurrent vascular disease such as diabetes. hypertension. However. There may be a shallow anterior chamber. Serial photographs and automated visual fields are more appropriate for managing this condition than IOP measurements. the glaucomatous mechanism is unknown. Laser trabeculoplasty and filtration surgery are often employed earlier than in POAG. Further. In terms of retinal vein occlusions. and GCA. Patients develop a secondary open angle glaucoma. The patient typically has significant corneal edema and elevated intraocular pressure. perform automated visual fields to look for preexisting field loss since pseudoexfoliative glaucoma undergoes periods of exacerbation and remission. retinal artery occlusion. topical carbonic anhydrase inhibitors.and branch retinal vein occlusion. In these cases.The development of glaucoma typically occurs due to a buildup within the trabecular meshwork of pigment granules and pseudoexfoliative material. Less common causes of NVG include hemi. there typically will be evidence of retinal vessel occlusion (either artery or vein). The most common causes of NVG include ischemic central retinal vein occlusion (CRVO). Only rarely will NVA develop without NVI. but more typically present with a chronically red. When first diagnosing pseudoexfoliation syndrome. Gonioscopically. There frequently is an antecedent history of a retinal vessel occlusion or chronic uveitis. ocular ischemic syndrome or diabetic retinopathy. Argon laser trabeculoplasty and filtration surgery are more effective in controlling IOP in cases of pseudoexfoliative syndrome than in POAG. Use topical betablockers. There will be visible neovascularization of the iris (NVI) and angle (NVA). Remember that pseudoexfoliative glaucoma undergoes periods of exacerbation and remission. often exceeding 50-mm-Hg. Treat pseudoexfoliative glaucoma in the same manner as primary open angle glaucoma. • Neovascular Glaucoma Signs and Symptoms Patients with neovascular glaucoma (NVG) may be asymptomatic. since the patient may experience progression yet manifest normal IOP if measured during remission.
BACTERIAL KERATITIS Signs and Symptoms The patient with bacterial keratitis will generally present with a unilateral. VEGF is theorized to diffuse forward to the nearest area of viable capillaries. there will be a modest amount of inflammation. Once in the angle. If a significant amount of the angle is in permanent synechial closure. acts to both physically block the angle as well as bridge the angle and physically pull the iris and cornea into apposition. In terms of retinal artery occlusions. a vasoproliferative substance. if NVG is due to ocular ischemic syndrome. and profuse tearing is common. namely the posterior iris. Neovascularization buds off of the capillaries of the posterior iris. which is the most common Culture-proven Pseudomonas keratitis with mucopurulent discharge. Miotics are absolutely contraindicated in any case where there is active inflammation. along the anterior surface of the iris. Retinal artery occlusions develop NVG in only 17 percent of cases and typically within four weeks post-occlusion. through the pupil.months of the occlusion. always consider GCA as a potential etiology. Aqueous suppressants may be used in order to temporarily reduce IOP. as well as a topical steroid such as Pred Forte. prescribe a topical cycloplegic such as atropine 1% b. Due to the extremely elevated intraocular pressure. thus blocking the trabecular meshwork. In cases of extreme retinal hypoxia. with acts upon healthy endothelial cells of viable capillaries to stimulate the formation of a fragile new plexus of vessels (neovascularization). hypoxia induces vascular endothelial growth factor (VEGF). Aqueous suppressants will temporize IOP and lead to a false sense of security as the neovascular process will continue with further angle closure. However. However. intensely injected eye. Prostaglandin analogs should likewise be avoided. or Flarex q. The result is a secondary angle closure without pupil block.i. There will be a focal stromal infiltrate with an overlying area of epithelial excavation. Visual acuity is usually reduced. filtering surgery must then be employed. there are essentially very few viable retinal capillaries available. minimize oxygen demand of the eye. PRP is less successful and 90 percent of these patients will have count fingers vision within one year. . and then into the angle. Vexol.d. This is best accomplished with panretinal photocoagulation to destroy ischemic retina. grows along the posterior iris. In that instance.i. photophobic.d. Clinical Pearls • • • • PRP has a 90 percent success rate in NVG due to diabetes if less than 270º of the angle is closed. PRP tends to be effective in causing regression and involution of anterior segment neovascularization. acutely painful. Management If there is any degree of inflammation and ocular pain. along with its attendant fibrovascular support membrane. chronic medical therapy is not indicated for neovascular glaucoma. Hypopyon in bacterial keratitis. In ischemic retinal disease. Often. and reduce the amount of VEGF being released. the neovascularization. NVG typically develops within four weeks of the occlusion. Peripheral anterior synechiae with permanent angle closure happens quickly. Ultimate management of NVG involves eradication of the vessels. In cases of NVG in elderly patients. there will be a history of contact lens wear.
and it appears that there is an increased incidence of Gram-positive recovery in infectious keratitis. often greatly out of proportion to the size of the corneal defect. The PMNs phagocytize and digest the bacteria and damage stromal tissue by releasing numerous enzymes that directly affect and damage stromal tissue. However. systemic immune disease. The collagen of the corneal stroma is poorly tolerant of the bacterial and leukocytic enzymes. As thinning advances. Intraocular pressure may be reduced due to secretory hypotony of the ciliary body. as well as sensitivity studies. are at risk of perforation.2 Pathogenic bacteria colonize the corneal stroma and immediately become antigenic. The conservative approach supports culturing most. The first step in management should be to obtain corneal scrapings for microbiologic studies. the most common infective organism is Pseudo-monas aeruginosa. chronic eyelid disease. which aggregate at the area of infection. thus introducing bacteria into the eye with ensuing endophthalmitis.4 If the patient has been cultured. if not all. but may be elevated due to blockage of the trabecular meshwork by the inflammatory cells. tear film abnormalities affecting the ocular surface and hypoxic trauma from contact lens wear. injection is typically 360 degrees rather than sectoral as seen in non-infectious keratitis. the cornea is prone to colonization and infection by pathogenic bacteria.1 Mucopurulent discharge may emanate from the lesion. A pronounced anterior chamber reaction. Pathophysiology Once the corneal defenses are breached. The results of this technique compared to platinum spatula collection and plating was 83. and undergoes degradation. and in institutionalized patients in nursing homes and hospitals where methicillin-resistant Staph. necrosis and thinning. The cornea may be edematous. initiate broad-spectrum. Monotherapy with fluoroquinolone eye drops has been shown to result in . The body mobilizes polymorphonuclear leukocytes (PMN). Factors known to compromise corneal defenses include direct corneal trauma. creating an infiltrate. The standard of care describes the use of a platinum spatula with plating directly onto blood and chocolate agar medium. In bacterial keratitis. often with hypopyon.precipitating condition. In cases involving contact lens wear and cosmetic mascara.3 Management Proper diagnosis and prompt therapy are essential to preserve vision in bacterial keratitis. suspected infectious ulcers. Identification. the effectiveness of the fluoroquinolones has led many practitioners away from this standard. This leads to scarring of the cornea. The most commonly occurring organisms in bacterial keratitis vary depending on the precipitating factors of the ulcer and the geographic location of the patient. aureus infections are possible. We advocate obtaining cultures for central lesions that threaten vision. both directly and indirectly. is present in severe cases. by releasing enzymes and toxins. the most common infective organism in bacterial keratitis is Staphylococcus aureus. Often. the eyelids will also be edematous. This sets up an antigen-antibody immune reaction with chemotactic factors inducing an inflammatory reaction.3% sensitivity and 100% specificity. An alternative for treatment of less severe keratitis is a mini-tip calcium alginate culturette and transport-media-containing carrier. The conjunctival and episcleral vessels will be deeply engorged and inflamed. will aid in management. the cornea may perforate. empirical antibiotic therapy prior to receiving the results. Throughout North America. Corneal trauma or pre-existing keratopathy are also common precipitating conditions.
then atropine 1% bid is indicated. This finding may have resulted from quicker clinical response of healing as a result of less toxicity found in the patients treated with fluoroquinolones. Allergan).6-8 consideration must be given to the increasing resistance to these drugs. If this is insufficient. Zymar or Vigamox dosed on an hourly basis may become the mainstay therapy for bacterial keratitis.1117 But note that steroids should not be employed until the antibiotic has been given enough time to sterilize the ulcer. The patient should be followed daily until the infection is well controlled.5% q2h can be added to speed resolution and decrease corneal scarring. It has been feared that the immunosuppressive effects of steroids could enhance bacterial replication and worsen infection. or if the patient shows signs of clinical improvement (the ulcer does not worsen. bacterial resistance to the second-generation fluoroquinolones has been increasing. and pain and photophobia are reduced) at the 24 to 48 hour follow-up visit.10 In the future. . Ocuflox (ofloxacin.3. while corticosteroids can inhibit the corneotoxic inflammatory response.5 Despite clear efficacy of fluoroquinolones in the management of bacterial keratitis.shorter duration of intensive therapy and shorter hospital stay when compared with combined fortified therapy (tobramycin-cefazolin). Antibiotics can suppress the infective organism. followed by two drops every 30 minutes for 18 hours. One also must be certain that there is not a simplex viral. However. deep ulcers in the elderly. Traditional initial monotherapy has utilized the fluoroquinolone Ciloxan (ciprofloxacin. there has been a rise in the incidence of bacterial isolates in keratitis that exhibit resistance to the early generation fluoroquinolones. While steroids have historically been avoided in the management of infectious keratitis. Another second-generation fluoroquinolone. Clinical Pearls • If a patient presents with a corneal infiltrate without overlying epithelial staining. If the results of cultures and sensitivities show that the initially prescribed antibiotic is appropriate for the infective organism.2. if the chosen antibiotic is effective against the organism.7 Both fluoroquinolones have been proven to be as effective for managing bacterial keratitis as the previously used fortified antibiotics. fungal. However. or protozoan infection prior to the initiation of topical steroids. moxifloxacin (Vigamox. two drops every 15 minutes for six hours.25% tid. as some serious complications were encountered more commonly in the fluoroquinolone group. and then tapered depending on patient response. steroids should only be used in conjunction with true bactericidal antibiotics such as fluoroquinolones. Strong cycloplegia is also mandatory in order to increase patient comfort and minimize inflammation.9 One method of combating the increasing problem of fluoroquinolone resistance and rising level of Gram-positive infections is to use the new fourthgeneration topical fluoroquinolones. Adjunctive use of cold compresses will also help to reduce inflammation. Unfortunately. Alcon) and gatifloxacin (Zymar. The two most recently available fourth-generation fluoroquinolones. then the condition may not be infectious bacterial keratitis. Since their inception. have a greatly lowered resistance rate while providing much greater Gram-positive activity than previous generation fluoroquinolones. is also an effective treatment for bacterial keratitis. minimally 24 hours. then the concurrent use of steroids will not inhibit the bactericidal effect of the antibiotic. judicious use can be beneficial.2. Alcon). a topical corticosteroid such as prednisolone acetate 1% or loteprednol etabonate 0. but with significantly fewer side effects. Also. The weakest cycloplegic that should be employed is scopolamine 0. caution should be exercised in using fluoroquinolones in large. Allergan). especially among the Gram-positive organisms.
Diseases associated with pannus • • • • • • • • • • • • • LASIK2 Allergic conjunctivitis3. For steroids to be most beneficial. then corticosteroid use will inhibit the inflammatory reaction and speed healing and reduce corneal scarring.11 Toxic conjunctivitis3 Neonatal conjunctivitis3 Chlamydial conjunctivitis3. If you wait until the ulcer re-epithelializes before adding a steroid.11 Fuch's endothelial dystrophy4. it is a finding that results secondary to another disease process. However. Pannus is not a diagnosis. In this instance.• • The use of strong bactericidal antibiotics will eliminate the infective organisms and sterilize the ulcer. ISK may be the initial manifestation of an unknown Active herpes simplex stromal keratitis. If there is evidence that the antibiotic is suppressing the infective organism. lacrimation.5 Congenital hereditary endothelial dystrophy6 Superior limbic keratoconjunctivitis of Theodore7 Terriens marginal degeneration7 Mycobacterial tuberculos pannus8 Leprosy8 Aniridia9 Keratoconjunctivitis10 Immune Stromal (Interstitial) Keratitis Signs and Symptoms Patients with active immune stromal keratitis (ISK) will present with pain. photophobia. the inflammatory reaction is as damaging to the cornea as is the infective organism. A cautionary note: Be comfortable that the antibiotic has sterilized the ulcer before instituting the steroid. it is pathologically defined as a superficial vascularization of the cornea with infiltration of inflammatory-connective-granulation tissue. usually within the first 24 to 48 hours after you initiate antibiotic therapy. prescribe them while the ulcer bed is still open.111 Pannus lesion. The presentation may be either unilateral or bilateral. . PANNUS Definition: The word "pannus" takes its origin from the Latin meaning "a piece of cloth. and blepharospasm. the beneficial effects will be reduced." Relating to the eye. active phase. but will do nothing to quell the inflammatory reaction. There will often be a history of ocular infection or systemic disease. Vision is typically reduced in the acute.
However.1 It must be emphasized that there is no active microbial infection within the corneal stroma in ISK. Although syphilis is the leading cause of inactive. indolent course and may persist for many months. and perforation. However. Acanthamoeba infection. the majority of herpetic ISK cases are non-necrotizing. the overlying epithelium is intact. sarcoidosis and onchocerciasis.1 Sixty percent of cases of bilateral. it is actually responsible for less than 20% of total cases. There are two types of ISK that may occur during herpes simplex infections: necrotizing and nonnecrotizing. active ISK are idiopathic in nature. Endothelial folds and keratic precipitates are common. Rather. prophylactic topical antiviral medications (trifluridine) should be used concurrently. and possible perforation. profound corneal thinning. When topical steroids are used to treat herpetic immune stromal disease. Lyme disease. measles. It must be remembered that ISK is an immune stromal keratitis and not an active infectious process. cheesy. however. it will be much smaller in area than the underlying inflammation. Non-necrotizing herpetic ISK does not have the same propensity to move toward ulceration. Pathophysiology ISK is an immune-mediated nonsuppurative stromal inflammation with an intact epithelium. thinning is not a distinctive feature. Cycloplegia and topical lubrication will ease the patient's discomfort.5 . Depending upon the etiology. There will be epithelial ulceration. When ISK is caused by the herpes virus.underlying systemic disease. The stromal vascularization will begin during the acute phase and progress throughout the disease's course. microbial antigens initiate a T-lymphocytic destruction of the stroma. accounting for over 70% of unilateral active cases. Lower doses of topical steroids may be employed to control the patients' disease and symptoms. syphilis. thinning. the presence of stromal vascularization is not required in order to make this diagnosis (as was previously thought). non-necrotizing ISK runs an indolent. mumps. However. dense vascularization. bilateral ISK. Management Immune stromal keratitis is a self-limiting condition. Occasionally. which will spontaneously resolve within several months. ISK runs a chronic. There will be a secondary anterior uveitis. the result invariably will be profound stromal vascularization and scarring with subsequent visual reduction. Corneal thinning may result as sequelae of the chronic inflammation. herpes zoster and simplex. Syphilis is the cause of approximately 50% of bilateral inactive cases. tuberculosis. treatment is indicated. Untreated. Hence. stromal edema. Typically. therapy deviates somewhat from the above-mentioned regimen. There will be a single or multiple white patches of infiltration and inflammation within the corneal stroma. self-limiting course over several months. Necrotizing herpetic ISK is a more severe form of herpetic stromal keratitis and manifests as a dense.2 Subsequent stromal vascularization and cicatrization invariably results if the underlying cause is left untreated. Conditions causing SK include Epstein Barr virus. ISK is typically associated with an often readily identifiable causative agent. the most common cause of active ISK is the herpes simplex virus. Fortunately. yellow-white stromal infiltration often following recurrent herpetic disease. If there is epithelial disruption. There will be concurrent stromal edema as well as stromal vascularization.3. the patient may need to use low doses of topical steroids indefinitely. Application of a strong steroid such as prednisolone acetate 1% q1h to q2h is optimal.4 There has been no proven benefit for the adjunctive use of oral acyclovir in the acute management of patients with herpes simplex stromal keratitis being treated with topical corticosteroids and trifluridine. ISK is idiopathic.
ataxia. As in other herpetic manifestations. the main identifiable cause of active cases of ISK is herpes simplex virus.g. Lyme titer for Lyme disease. the patient should receive medical treatment directed toward the underlying cause while he or she undergoes topical treatment. In cases of active herpetic ISK. Historically. inflammation of other ocular structures. vertigo. Patients with dry eye commonly present with complaints of ocular irritation or discomfort. However. Meniere's-like attacks. In this case. permanent deafness may result if systemic steroid therapy is not promptly instituted for audiovestibular dysfunction. Stromal inflammatory infiltration in herpetic ISK can be difficult to differentiate from both bacterial and fungal keratitis. inactive ISK.9 Clinical Pearls • If a patient develops ISK on the same side as a prior episode of either HSV or HZV and there is no indication of other disease in the patient's history.Herpes simplex ISK is a highly recurrent disease.. Although the ocular manifestations respond to topical steroids and are rarely serious. • • • • • DRY EYE SYNDROME Signs and Symptoms Dry eye syndrome may occur in a wide range of individuals. it can safely be assumed that the cause of the ISK is herpetic. PPD and chest X-ray for tuberculosis. As Generalized injection associated with moderate dry eye. . IK will have a more intact epithelium whereas the other entities will have ulceration. but also stromal disease. while major morbidity and even death may occur if systemic sequelae such as vasculitis and aortic insufficiency are not recognized. or aortic insufficiency. Unless the cause is obviously herpetic. rheumatoid arthritis.7. IK runs an indolent course. ISK has been associated with syphilis as the main causative agent. and rheumatoid factor and antinuclear antibodies for collagen vascular disease. however. Particular attention must be paid to patients presenting with ISK and hearing loss. Suspect Cogan's syndrome in patients presenting with ocular inflammation who develop hearing loss. signaling Cogan's syndrome. audiovestibular dysfunction or systemic vasculitis. and those with connective tissue disorders (e. The only use for either oral or topical antiviral medications in herpetic IK is prophylactically to prevent epithelial ulceration when topical corticosteroids are used and to suppress future recurrences. Sjögren's syndrome). whereas infectious keratitis is much more aggressive. a diagnostic evaluation should be initiated. As ISK can result from a variety of causes. the elderly. tinnitus. Cogan's syndrome is an idiopathic inflammatory disease. which may present as ISK. topical and oral antiviral medications have been exceedingly disappointing therapeutically. medical evaluation for IK should include FTA-ABS or MHA-TP for syphilis. corneal sensitivity is reduced on the affected side. although it is more frequently seen in women. then no further diagnostic evaluation is necessary.8 Strong consideration should be given for long-term suppressive therapy beyond one year in herpes simplex stromal keratitis. syphilis is the main cause only in cases of bilateral. Today. Should a cause be elicited. with the risk related to the number of previous recurrences. Further. By far. vasculitis.6 Long-term suppressive oral therapy with acyclovir 400mg po bid has been shown to significantly reduce the recurrence rate of not only epithelial keratitis from herpes simplex.
The condition tends to be categorized as either "tear deficient" or "evaporative.g. Conditions involving mucin or lipid deficiencies (e. Negative corneal staining from surface disease in dry eye.11 Management ." based upon a comprehensive classification scheme that was developed in 1995. Additional clinical tests for dry eye syndrome are numerous. Filaments. researchers have shown a significant link between androgens and dry eye. Upon gross inspection.24 This is supported by the fact that pro-inflammatory cytokines and activated T cells have been identified in the lacrimal glands of both Sjögren's and non-Sjögren's patients. and may be ascertained by use of Schirmer tear test strips or the Zone-Quick test. altered blink reflex. Another device. revealing startling new information. in association with the discomfort. However. lysozyme analysis. low humidity or extreme heat. Of the more intriguing theories is that dry eye may be the result of an inflammatory process within the cornea and/or lacrimal glands. More involved and invasive procedures. dryness is the most frequently cited problem. possibly due to suppression of endogenous androgens by increased estrogen levels. Occasionally. such as Sjögren's syndrome or lacrimal gland disease.8. which are tags composed of mucus. or a "sandy/gritty" foreign body sensation. Pathophysiology Dry eye syndrome has traditionally been viewed as a quantitative or qualitative reduction in the precorneal tear film. key slit lamp findings may include a meager tear meniscus at the lower lid. Sodium fluorescein staining may be evident as punctate epithelial keratopathy from the interpalpebral region to the lower third of the cornea. constitute the tear. a great deal of research has been conducted in the area of dry eye. Tear volume assessment is used quite commonly.1 Those conditions that contribute to diminished tear production.deficient variety. low environmental humidity. these sex hormones may help regulate homeostasis of the tear secretion process. or other surface disorders comprise evaporative dry eye. the Keeler Tearscope. patients will report excess lacrimation. may be useful in quantifying dry eye for research purposes. particularly the lipid layer. Over the last several years. and tend to be more prominent later in the day. a form of dry eye syndrome.9 Apparently. generally less than ten seconds.. may also stain with these vital dyes.5. or epiphora. Dimin-ished "wetting" of these test media over a set period of time (five minutes for the Schirmer and 15 seconds for the Zone-Quick test) is indicative of tear volume deficiency.7 On another front. with a multitude of etiologies and contributory factors.6 In addition. rose bengal or lissamine green staining of the cornea and/or conjunctiva may be seen in the same area. Stevens-Johnson syndrome or blepharitis). Women who take hormone replacement therapy with estrogen have an increased incidence of dry eye. as well as a reduced tear break-up time (TBUT). Other contributory factors may include contact lenses. In more severe cases. lactoferrin assay. burning. and impression cytology. irregular ocular surface topography. patients may further report itching. and high altitude. moderate to severe dry eye states have been seen to respond favorably to treatment with corticosteroids. but they are hardly practical for routine clinical diagnosis.the name implies. Symptoms may be exacerbated by poor air quality.10. the majority of these patients demonstrate a relatively white and quiet eye. epithelial cells and tear debris. utilizes interferometry to evaluate the thickness of the tear film components. including tear film osmolarity.
Clinical Pearls • The symptoms of dry eye syndrome tend to be quite variable. They are utilized by some physicians for advanced KCS.16 Patients with keratoconjunctivitis sicca (KCS)." Although this topical drug may require bid dosing for up to six months to achieve maximum efficacy. These muscarinic agonists stimulate non-selective secretion from exocrine glands via autonomic pathways. a significant percentage of plugs may be spontaneously expelled. citing the new inflammatory theories of dry eye. The immunomodulatory agent Restasis (0. Astute clinicians realize that the diagnosis of dry eye is more often based on subjective complaints than on ocular inspection.. In general.14. may not respond to any topical therapy. whose tear production is presumed to be suppressed due to ocular inflammation." on page 34A). they should be dosed frequently (at least every hour). management of dry eye syndrome has been aimed at replenishing the eye's moisture and/or delaying evaporation of the patient's natural tears. rather than alleviates.15 Some individuals have actually cautioned against occlusion therapy in many cases.Historically. These may include antihistamines. in some cases. significant causes of evaporative dry eye syndrome. phenothiazine antianxiety preparations. SnowBrand Pharmaceuticals). damage to the ocular surface. While the theory is sound. FDA "for patients with keratoconjunctivitis sicca . artificial tears may be used as frequently as necessary. Often.. although some are only indicated for qid use. Also. creating or exacerbating a dry eye state. to promote healing of the ocular surface epithelium. diuretics. Allergan) has recently been approved by the U. beta-blockers. however this is not currently an FDAapproved application of these drugs. resulting in enhanced tear production. the use of oral omega-3 fatty acid supplements has been suggested as a less invasive way to improve meibomian gland function and tear stability. Typically these agents are used for xerostomia (dry mouth) associated with Sjögren's syndrome or certain forms of cancer. a more severe form of dry eye. and practitioners should familiarize themselves with the various options (see "Overview of New Dry Eye Products. MGI Pharma) and Evoxac (cevimeline HCl 30 mg. Often.05% cyclosporine A ophthalmic emulsion. The use of oral tetracycline therapy (e. and it has been noted that many patients notice a subjective decrease in improvement of symptoms with the plugs over time.g. oral contraceptives. The first line of defense typically involves the use of ophthalmic lubricants ("artificial tears"). and then tapered based upon patient response and compliance.. • . they suggest that the use of punctal plugs actually creates a "cesspool" of cytokines and promotes. When beginning therapy. patients seem to be more symptomatic than their clinical signs would indicate. doxycycline 100mg bid x six to 12 weeks) may be beneficial in patients who fail to improve with lubricating drops and lid hygiene. The purpose of these agents is to alleviate symptoms and.13 Lacrimal occlusion with punctal or intracanalicular plugs offers a different management strategy for dry eye. essentially preventing drainage of the tear film and maximizing contact duration with the ocular surface.12 Oral medications and nutritional supplements have been utilized with success for patients with blepharitis and meibomian gland disease. Patients who do not respond to palliative therapy may require more substantial treatment in the form of topical and/or oral pharmaceutical agents. these patients benefit from oral secretagogues such as Salagen (pilocarpine HCl 5 mg.S. many antidepressants and atropine derivatives. A great deal of diversity exists within this market. it has been shown to ameliorate symptoms in up to 44% of patients and improve basal tear production (as demonstrated by Schirmer testing) in up to 59% of patients. Many common systemic drugs can transiently decrease lacrimal secretions.
bleph-arospasm.111 Biomicroscopy of the injured area often reveals diffuse corneal edema and epithelial disruption. Descemet's membrane. The newly created wound appears as a bright green area compared to the rest of the cornea because the dye accumulates in the divot. the wing cell layer. Patients usually present with some or all of the following: acute pain. folds in Descemet's membrane may be visible.8 Bacteriologic examination of lenses at the time of the event demonstrated the association. Abrasions may result from foreign bodies. and finally the endothelium. contact lenses. CORNEAL ABRASION Signs and Symptoms Corneal abrasion is one of the common clinical entities that present to the optometric practice. not involving Bowman's membrane and deep. Cobalt blue light inspection. but not rupturing Descemet's membrane. The cornea has remarkable healing properties.5 Recent data suggests that the integrity of the basement membrane following the injury is a deciding factor in determining the regenerative character of the corneal repair. containing the corneal nerves and the mitotically active basement membrane. 250 lamellar sheets of stroma. The cornea has five distinct layers.3. when edema is excessive. will illuminate the denuded epithelium. foreign-body sensation. chemicals.5. fingernails.8 In one study. In severe cases. care and lens cleanliness. that this is a chronic disease. usually within 24 to 48 hours.8 . The only way for patients to achieve control of their symptoms and discomfort is through active participation in the prescribed treatment regimen and periodic reevaluation. Below the tears lies the corneal epithelium.7 For years contact lenses have remained at the top of the list of consumer goods known to perpetrate ocular injuries. Lesions that extend below Bowman's membrane possess an increased risk for leaving a permanent opacity. following the instillation of sodium fluorescein dye. Further. There is no "magic bullet" cure. ulceration following contact lens-induced corneal abrasion has been recognized and demonstrated as a secondary phenomenon to suspect compliance. marked by exacerbations and remissions. dust and the like. adding density. tree branches. practitioner and patient alike must understand one basic tenet of dry eye management: namely. Below the epithelium is the Bowman's membrane (a structure designed to prevent penetrating injuries). The epithelium adjacent to any insult expands in size to fill in the defect. hair brushes. There are two categories of corneal abrasion. lacrimation.• Before initiating any form of therapy.5 Lesions that are purely epithelial often heal quickly and completely without scarring.10 Pathophysiology Corneal abrasion without fluorescein. perseverance and a willingness to try new (and sometimes unconventional) options. superficial. aureus. photophobia. ulcers were found only in corneas that were scratched with contact lenses colonized by viable S. blurry vision and a history of contact lens wear or being struck in the eye. and appropriate care requires patience. penetrating Bowman's membrane. The corneal epithelium is actually composed of three tissues: the stratified surface epithelium.
A dilated examination should be completed to rule out posterior effects from the trauma.15 Clinical Pearls • • • • To prevent recurrent erosion and reduce corneal edema.1. Alcon) or a fluoroquinolone (Vigamox. Any anterior chamber reaction should be observed and noted as well. 9. or prevent the moisture already present from evaporating too quickly.10 Patching must always be avoided in patients who wear contact lenses due to the threat of microbial keratitis. The eye examination should proceed in a logical fashion from external adenexa to funduscopic examination. qid) or a thin. There was no significant difference in percent healing between the two groups. The abrasion should be documented for size. topical steroids may be required. Consistent with the data of others. a cotton-tipped applicator saturated with anesthetic may be used to debride loose tissue. 11 Pressure patching is no longer considered standard-of-care. 10. gentamicin or Tobrex (tobramicin. Bed rest. Patients should be reevaluated every 24 hours until the abrasion is reepithelialized. low water content bandage contact lens can be prescribed. Moist Eye . The Seidel test (painting of the wound with dye observing for aqueous leakage) is used to uncover full-thickness injuries.1 Freeman introduced the first silicone punctal plug in 1975.2 and other devices to prevent surface evaporation (e. even when adjusted for age and initial abrasion size. Worsening subepithelial infiltration may be a sign of infection. Lesions such as these should be considered vision threatening. place and activity surrounding the injury should be recorded for both medical and legal purposes. location and depth. pressure patching for corneal abrasions provides no benefit. Zymar).Management Treatment for corneal abrasion begins with history. inactivity and over-the-counter analgesics can be used to quiet acute pain. warranting immediate treatment with fluoroquinolone antibiotic drops and consideration for culture. Allergan).2. a hypertonic solution or ointment may be prescribed along with the other medications or after reepithelialization has occurred. shape.5 When significant secondary uveitis is present. anesthetic) should be instilled to identify the corneal defects. Medical treatment is initiated by using adequate cycloplegia (the potency of which should be determined on a case-by-case basis) and topical antibiotics such as Polytrim (polymyxn B and trimethoprim. The time. topical nonsteroidal anti-inflammatory medications (Voltaren or Acular. If the blepharo-spasm is sufficiently intense to preclude an acuity measurement. The eyelids should be everted and fornicies scrutinized to rule Corneal abrasion with fluorescein out the presence of foreign material.16. Ophthalmic lubricating solutions. The VA should be measured immediately thereafter. have remained the mainstay of dry eye therapy since their introduction in the 1940s. there were only two options for managing dry eye syndrome: either put more moisture into the eye.g. In cases where pain is severe. one drop of topical anesthetic from a recently open bottle can be administered. more commonly known as artificial tears.3 OVERVIEW OF NEW DRY EYE PRODUCTS FOR MANY YEARS.5 In cases where excess epithelium impairs regrowth. Fluorescein dye (without staining.46. Visual acuity (VA) should be recorded before any procedures or drops are given.10 Researchers examined patients with corneal abrasion: 17 with an eye patch and 18 with no eye patch. if possible.
It is preservative-free and packaged in single-use. and Refresh Tears (Allergan. The biggest issue is duration of action. etc. manufacturers have introduced several preservative-free solutions and "disappearing preservatives" to address the issue of toxicity. This is an intriguing theory. a small company based in Oregon launched a unique product that has captured the interest of many exhibit hall attendees. Allergan decided to manufacture this unique vehicle. preserved with Purite). Hypotears PF. Nature's Tears is sprayed toward the eyes from a distance of 12 to 18 inches. Tears Naturale PF. but only three product lines contain preservatives that break down soon after instillation. there is a lack of significant prospective studies demonstrating that this product is any more effective than other artificial tear supplements. Therefore. Endura is the first lubricant eye drop for dry eye that treats all three layers of the tear film. patients frequently report only fleeting relief (on the order of five to 10 minutes) after instillation of many tear supplements. A cursory review of an online health product service (www. Trends in Artificial Tears Despite their popularity and success. The following is a review of some of the more recent products introduced for therapy of dry eye syndrome. manufacturers have begun producing thicker. TheraTears Liquid Gel (Advanced Vision Research). preserved with Dissipate). claims the manufacturer. two significant difficulties still exist with artificial tears. Nature's Tears In mid-2002. and the product possesses a significant novelty factor. Undaunted.). as well as diminished symptoms of dryness and irritation in patients using the solution two to four times daily over 90 . but these modalities have never been able to supplant artificial tear therapy from its #1 position. Nature's Tears mist allows for replenishing of the aqueous component without disturbing the other tear layers. However. and market it directly to the public as an over-the-counter product. Endura In the summer of 1999. The premise? Artificial tears flood the ocular surface. Also. or sodium perborate). an emulsion of castor oil and lubricants in an aqueous solution. Refresh Endura was launched. and hence there was no significant difference between the controls and the study group. disposable vials. the FDA Ophthalmic Drugs Subcommittee advisory panel unanimously recommended not to approve Allergan's formulation of topical cyclosporine for the treatment of keratoconjunctivitis sicca. GenTeal Gel (Novartis). One of the reasons cited was that the solution vehicle showed very similar efficacy to the drug itself. and Systane (Alcon). In the fall of 2002. Examples of such products include Refresh Liquigel (Allergan). However. which can be a significant source of toxicity. it can be frustrating and intimidating for both patients and practitioners to know which option to select.g. Virtually every line of dry eye products includes a preservative-free version (e.com) reveals over 50 distinct items when the term "artificial tears" is entered in the search engine! With so many products to choose from.moisture panels from EagleVision) have joined the ranks over the years.drugstore. washing away the lipid and mucin layers and depleting normal enzymes. Nature's Tears (Bio-Logic Aqua Technologies) is described by the manufacturer as an all natural moisturizing mist for the eyes consisting simply of tissue culture grade water with no preservatives or propellants. Also of concern is the addition of preservatives in many artificial tears. Controlled clinical trials with Endura showed enhanced fluorescein tear break-up time.. more viscous agents that increase corneal contact time without blurring vision. According to Allergan. preserved with GenAqua. particularly when these preparations are used frequently. These include: GenTeal (Novartis. Rather than being instilled as a drop. Tears Again (Cynacon/Ocusoft.
too uncomfortable or too expensive. Personal experience with Systane has shown it to be an outstanding choice for patients with moderate to severe dry eye who are not ameliorated with normal viscosity tear solutions. allowing the epithelial cells to heal and reestablish healthy microvilli and a normal glycocalyx. the time frame of six months may seem irrationally long for some practitioners and patients to observe improvement in the disease course (even though many patients experience improvement after only a few weeks). rather than only temporarily alleviate symptoms. HP guar binds to the ocular surface and simultaneously crosslinks with borate ions in the solution. the fact remains that Restasis may offer great potential benefit to many of our patients." In clinical studies. particularly suited for patients with lipid deficiencies secondary to meibomian gland dysfunction. It is also excellent for managing minor corneal trauma or exposure keratopathy.05% cyclosporine ophthalmic emulsion) for the treatment of keratoconjunctivitis sicca. In a randomized. Therapies on the Horizon .4). a reduction in conjunctival T-lymphocyte infiltration was noted after six months of cyclosporine therapy.5 Third.6 Allergan heralds Restasis as the first drug proven to effectively treat a cause of dry eye disease.4 Mild blurring for 30 seconds after instillation was the most significant adverse effect. the FDA approved Restasis (0. Alcon introduced a unique artificial tear product. but when placed in the eye (which has a pH of ~7. the retail cost of Restasis is somewhat expensive as compared to conventional therapy. provides extended relief of dry eye symptoms and generates a protective coating on the ocular surface. according to Alcon. Systane is a liquid in the bottle at a pH of 7.. dry eye patients receiving Systane four times daily for six weeks showed a statistically significant reduction in surface staining. Systane In early 2003. on the order of $80 to $100 per month. Restasis is prescribed on a bid basis. ocular burning has been reported as an adverse event in up to 17% of individuals utilizing the drug. Second. this coating serves as a temporary corneal bandage. forming a network with a gel-like consistency. But although this product has yielded good results in clinical trials. controlled clinical trial.5 Additionally. which utilizes the demulcent technology of hydroxypropyl (HP) guar.whose tear production is presumed to be suppressed due to ocular inflammation. This change is based on pH value. increases in viscosity after contacting the ocular surface. as well as increased tear break up time. Finally.0.. Restasis In December 2002. Clinical practice has shown it to be an excellent and well-tolerated solution. While these issues cannot be ignored. In theory. a chemical reaction occurs.days.3. making it the first commercially available pharmaceutical therapeutic agent for the treatment of dry eye. This topical solution is classified as an immunomodulatory agent by the manufacturer (Allergan). practitioners have been somewhat reluctant to actively prescribe Restasis for several reasons. and is approved "for patients with keratoconjunctivitis sicca. Restasis was shown to ameliorate symptoms in up to 44% of patients and improve basal tear production (as demonstrated by Schirmer testing) in up to 59% of patients after six months of treatment. dryness and foreign-body sensation. many are confused as to precisely which dry eye patients will benefit from this therapy. Practitioners need to remain open minded and personally evaluate this product on at least a few patients before reaching the conclusion that it is too slow. The result is a more viscous ocular lubricant that. Systane. First.
water and mucin from conjunctival cells. there will be no hemorrhage unless choroidal neovascularization has developed. of direct or contrecoup injury to the eye and surrounding structures. However. there may be hemorrhage in any layer ranging from the choroid to the vitreous. but will resolve. and received an approvable letter from the FDA on December 22.7 Inspire Pharmaceuticals filed a new drug application for INS365 in June 2003. However. a topical agent referred to as INS365 Ophthalmic by Inspire Pharmaceuticals. in that it induces secretions from bodily tissues.7. There is usually significant reactive RPE hyperplasia. Pathophysiology Direct or contrecoup injury can precipitate a choroidal rupture. Hemorrhage and edema may be present initially. Diquafosol tetrasodium. Often. In recent trauma. Visual acuity and visual field may be dramatically reduced or may be normal and the patient is asymptomatic. either recent or antecedent. . Choroidal ruptures may be single or multiple and may affect any part of the posterior segment. Often. Like INS365.More products remain under investigation for the treatment of dry eye syndrome. 2003. if the trauma was many years antecedent. choroidal neovascular membranes may develop within the rupture. when instilled in the eye. effectively creating an artificial tear comprised of purely endogenous components. if the RPE is disturbed and becomes hyperplastic and invades the sensory retina.8 These receptors are believed to regulate a variety of cellular responses. INS365 has been shown to pull salt. enhancement of this element may help to alleviate corneal injury and restore corneal integrity in dry eye patients. has been shown to activate P2Y2 receptors in the mucosal cells of the palpebral conjunctiva. the overlying retina is undisturbed in choroidal rupture. Specifically. Typically. Choroidal Rupture Signs and Symptoms Patients who experience choroidal rupture are often younger and involved in activities. visual dysfunction ensues. giving the rupture a pigmented appearance. the rupture will have the concave aspect toward the disc. you will note a linear disruption that may be crescent-shaped. reactive hyperplasia gives the rupture a heavily pigmented appearance. Patients have a history. When used topically on the ocular surface. 15(S)-HETE stimulates production of the glycoprotein Muc1.9 Muc1 is an important component of the tear mucin layer. Still in clinical trials is 15(S)-HETE (15-hydroxyeicosatetraenoic acid) from Alcon Laboratories. A launch of this product is anticipated sometime in 2004. such as ball sports. Due to the subsequent disruption of Bruch’s membrane that occurs in choroidal rupture. which expose them to potential high-rate impact trauma to the eye or adenexa. Ophthalmoscopically. this product is best described as a secretagogue. This may be a late development that can occur up to five years after the precipitating trauma.
laser photocoagulation is indicated only if there is imminent threat to vision. usually saliva. but quickly coalesce to form the familiar branching patterns which stain brightly with sodium fluorescein dye. accompanied by stromal keratitis in more severe presentations. depending upon the location and extent of the corneal lesion. but these are less common with recurrent HSV. Any late bleeding should receive a fluorescein angiogram to determine if a choroidal neovascular membrane has developed. As the cells die. and may affect the skin and mucous membranes of the host. Management Corneal epithelial disease secondary to HSV infection must be managed aggressively and quickly to . Monitor the patient funduscopically for at least five years for the development of choroidal neovascularization within the rupture scar. A dendritic corneal ulcer is the hallmark sign of HSV infection. conjunctivitis and uveitis are common sequelae. trauma. the leading edges (the so-called "terminal end-bulbs") will stain with rose bengal or lissamine green. Clinical Pearls • • • Choroidal neovascularization can occur five years after the initial trauma. It is transmitted via bodily fluids. Educate patients about their condition and prescribe protective eye wear. As the retina overlying a choroidal rupture may be unaffected. Photophobia and epiphora are common. Choroidal neovascular membranes resulting from choroidal rupture have a tendency to spontaneously involute. the virus remains dormant in the body of the host and can be reactivated in as many as 25 percent of cases by fever. You may see a vesicular skin rash and follicular conjunctivitis with the initial infection. immunosuppressive agents or exposure to ultraviolet radiation. Disciform stromal scarring. sometimes affecting the skin of the lids but more commonly resulting in a "fever blister" or "cold sore" in or around the mouth. Herpes Simplex Keratitis Signs and Symptoms The keratitis caused by the herpes simplex virus (HSV) typically presents as a unilateral "red eye" with a variable degree of pain or ocular irritation. It typically manifests as a vesicular rash. After resolution. patients may retain excellent visual function and present asymptomatically years after the trauma.Management There is no direct intervention in the acute phase of choroidal rupture. Primary infections occur most often in children between the ages of 6 months and 5 years. Sub-retinal hemorrhage from choroidal neovascularization is the most common cause of late vision loss. A patient may have a rupture between the disc and macula. an ulcerative keratitis results. These ulcers may begin as nondescript punctate keratopathies. For this reason. In recurrent attacks. the virus invades and replicates within the corneal epithelium. A more common sign is secondary uveitis. however. Because the virus invades and compromises the epithelial cells surrounding the ulcer. stress. vision may or may not be affected. Pathophysiology Herpes simplex is actually the most common virus found in humans. yet retain normal acuity.
.25% b. however. toxicity seems to be low. but this has not been definitively proven to hasten resolution or improve the final visual outcome. At this point. You may also need to prescribe a cycloplegic (homatropine 2% t. scattered multiple areas of sub-epithelial and anterior stromal infiltrates. Place the ointment in the lower cul-de-sac five times per day at four hour intervals. again depending upon the severity of the uveitic response. with or without epithelial defects. and usually do not warrant much concern.i. At this point. Studies show that the virus replicates more rapidly in the presence of steroids. The treatment of choice is topical trifluridine 1% given at two hour intervals. Accompanying sequelae may include mild iritis. Frequently the patient will provide an ocular history of having a dry eye and a systemic history of rheumatoid arthritis or other collagen vascular diseases. consider a history of prolonged sun exposure or extreme psychological stress to be significant in diagnosing HSV. Some practitioners recommend debriding the ulcer bed to remove active virus cells. have the patient continue the medication t.e. leading to hypoesthesia (reduced corneal sensitivity).d. particularly if the individual has a previous history of similar "infections. prolonging the course of the disease. significantly reduces the recurrence of herpes simplex keratitis in imunocompetent patients. little to no conjunctival chemosis.i. Patients with Staphylococcal hypersensitivity reactions may present without symptoms. vitamin A-deficiency and contact lens solution reaction.d. Avoid topical steroids in cases of active epithelial HSV keratitis. One or more marginal subepithelial corneal infiltrates are common in many conditions. marginal sub-epithelial infiltrates secondary to contact lens wear and Mooren's marginal corneal ulcer. for another week to ensure suppression of the virus.d. marginal sterile corneal ulcer patients present with only mild conjunctival injection.d.prevent deeper penetration. consider using oral prophylaxis therapy only in patients with confirmed recurrent HSV keratitis or patients on initial presentation who request it after being thoroughly educated. taper the dosage to q3-4h until the lesion resolves completely (usually in seven to 10 days). The entity is usually bilateral. Sterile Corneal Infiltrates SIGNS AND SYMPTOMS Unlike bacterial corneal ulcer patients. As the dendrites begin to regress..i. A new development in the management of herpes simplex keratitis has come in the form of topical acyclovir ointment (Zovirax). nine times daily. Also. The principle differential diagnoses include infectious corneal ulcer.-q.i.-q. Other known associations are vernal keratitis. folds in Descemet's membrane if there is substantial corneal edema. the patient seems to be in far less discomfort than the appearance of the eye would indicate)." Each recurrent attack induces greater damage to the corneal nerves. At this point. Clinical Pearls • • Suspect HSV in cases of unilateral adult-onset red eye that is inconsistent with the symptoms (i.d. The use of oral acyclovir (400mg 5x/day) or another oral antiviral for recalcitrant ulcers has yet to be proven clinically significant.i. use it whenever in doubt. One distinct characteristic is the notable clear zone that lies between the areas of infiltrate and the limbus. line the limbal area (mostly inferiorly). it has been shown recently that the use of oral acyclovir 400mg q. Here. and posterior synechiae in chronic cases. ocular irritation and normal vision. or scopolamine 0.d. However.). The cotton-wisp test for corneal sensitivity is invariably positive in cases of HSV keratitis.
or occasionally severe pain. aureus is recognized as one of the common opportunistic ocular pathogens. Nevertheless. CLINICAL PEARLS • Since the corneal tissue is free from infection and its damage originates from the secondary effects of inflammation. Sometimes. the discomfort is described as a scratchiness or the aptly named “foreign-body sensation. the involved eye may demonstrate lid edema. Many practitioners are apprehensive about prescribing topical steroids in the face of corneal epithelial compromise. begin with antibiotic treatment alone for 24 to 48 hours. although this does not usually pose a serious threat. MANAGEMENT The treatment strategy for marginal sterile keratitis is two-fold: (1) control and eradicate the microorganism and (2) control and eliminate the destructive elements and sequelae of inflammation. and a mild to moderate anterior chamber . Staphylococcus aureus.. Eyelid scrubs BID/TID using commercially available lid scrubs or baby shampoo will begin the process of cleansing the lid margins. Upon inspection. prescribe a cycloplegic. If the patient complains of discomfort. Polymorphonuclear leukocytes and fibroblasts. the microorganism must be able to adhere to the corneal surface. Rx a topical steroid based on the severity of the condition. In addition to its ability to infect the central cornea. Today. many believe it is only necessary when a condition fails to respond to the prescribed therapy. possibly accounting for their more frequent involvement in corneal disease. Streptococcus pneumoniae and Pseudomonas aeruginosa are significantly more adherent than other organisms. • Corneal Foreign Body SIGNS AND SYMPTOMS Patients who experience a foreign body of the cornea generally present with mild. prescribe a topical aminoglycoside (gentamicin. The organism is a grampositive non-encapsulated coccus capable of producing a variety of exotoxins and enzymes. tobramycin) or fluoroquinolone (ciprofloxacin. For bacterial infection or inflammation to occur. norfloxacin. Powerful exotoxins released by bacteria colonizing the eyelid margin induce peripheral corneal destruction through antigen-antibody reactions.” Excessive tearing. the most expeditious treatment is both topical antibiotics and topical antiinflammatories. blurred vision and photophobia are also common complaints.PATHOPHYSIOLOGY Sterile infiltrates usually represent a low-grade immune response to bacterial exotoxins. if you prefer a more conservative approach. produce collagenase and proteoglycanase enzymes that often produce additional damage. The antibiotics kill the bacteria and also mechanically wash organisms and their toxins away from the eyelid margin. These organisms are more adherent to the cornea and are tightly adherent to themselves. Because culture results are not available for 24 to 48 hours. ofloxacin) QID. focal or circumlimbal conjunctival injection. moderate. then judiciously add a topical steroid thereafter and monitor for IOP rise. Staph. providing a resistance to phagocytosis by host inflammatory cells. To fully eradicate dense colonies of lid margin bacteria. which migrate to the area to help fight exotoxins. it is a leading cause of sterile marginal keratitis. We advocate treating immediately and then culturing if the condition does not improve or worsens within the first 48 to 72 hours. there is debate regarding the need to culture before starting treatment.
this conversation should be well documented to avoid negative clinico-legal ramifications. If this is not possible simply with slit lamp inspection. Other associated findings may include lens dislocation. use a flexible-loop foreign body spud or 25-gauge needle to remove the object under the slit lamp. If the foreign body is metallic. CLINICAL PEARLS • • When a corneal foreign body encroaches the visual axis. you’ll often see a rust ring surrounding the object. for example. remove the object under topical anesthesia (1-2 gtt 0. and hyphema. Patients are photophobic and lacrimate profusely. A direct stream of sterile irrigating solution may be sufficient to dislodge some small foreign bodies.5% proparacaine). If this is not successful. The most critical sign is the finding of particulate matter at the surface of or embedded within the cornea. iridodialysis. CORNEAL LACERATION Signs and Symptoms The patient with a corneal laceration has experienced significant ocular trauma. if not removed. counsel patients as to the potential loss of acuity due to unavoidable scarring. There may be either a full thickness laceration or a partial thickness laceration. (Fingernail scratches. typically from a metallic object impacting with sufficient force. you may see a ring infiltrate surrounding the site. conjunctiva and cornea. If the foreign object remained embedded in the cornea for 24 hours or more.) There is intense pain initially which may diminish slightly due to corneal desensitization. before proceeding. The foreign object sets off an inflammatory cascade. There is significantly reduced visual acuity. typically from a metallic object such as a hand tool. can cause infection and/or tissue necrosis. it is important to ensure that the object has not perforated the cornea. you must instill fluorescein to inspect for aqueous leakage through the wound (Seidel’s sign). If there’s no penetration. Intraocular pressure generally ranges from 2 to 6 mmHg. There is a significant attendant uveitis and the anterior chamber is shallow or even flat in a full thickness laceration.reaction. Small particles may become lodged in the corneal epithelium or stroma. A full thickness laceration is termed a penetrating . Bubbles within the anterior chamber are a key finding. Pathophysiology A corneal laceration results from direct trauma to the cornea. resulting in dilation of the surrounding vessels and subsequent edema of the lids. White blood cells are also liberated. If you are unable to rule out the possibility of a penetrating ocular injury. PATHOPHYSIOLOGY Corneal foreign bodies generally fall under the category of minor ocular trauma. apply a shield to the eye and refer the patient immediately to a nearby hospital or ophthalmology practice. resulting in an anterior chamber reaction and corneal infiltration. A foreign body. particularly when projected toward the eye with considerable force. do not usually have enough force to lacerate a cornea. MANAGEMENT Initially.
Changes in visual acuity will depend upon the severity and stage of the disease. a shallow or flat anterior chamber or the presence of bubbles within the anterior chamber indicates a breach in the corneal integrity. Management The diagnosis of corneal laceration must be made as quickly as possible with as little intervention as possible. abnormal thirst (polydypsia) and abnormally frequent urination (polyuria). Intraocular pressure measurement should be avoided in any cases suspected to be full thickness lacerations. and shield the eye gently for protection while the patient is in transit to the surgeon. Visual acuity must be taken. Arrange for the corneal laceration to be surgically repaired by a corneal specialist immediately. In full thickness lacerations. A topical antibiotic solution may be judiciously applied. DIABETIC RETINOPATHY SIGNS AND SYMPTOMS A microvascular disease that primarily affects the capillaries. Clinical Pearl • • • With full thickness corneal lacerations. Use an eye shield to protect the eye. Assess the injury. Judicious use of a topical anesthetic will alleviate patient discomfort and allow the clinician to make an appropriate diagnosis. Again. Swelling within the crystalline lens results in large sudden shifts in refraction as well as premature cataract formation. Additionally. you will see the aqueous oozing out from the wound amidst the fluorescein. neovascularization elsewhere . Of course. Patients may present with histories of long-standing injected bulbar conjunctivae along with systemic complaints of weight loss despite larger than normal appetite (polyphasia). diabetes mellitus affects the eye by destroying the vasculature in the conjunctiva. a partial thickness laceration must be differentiated from a full thickness laceration with the use of Seidel’s test. exudates. Absolutely avoid pressure patch or bandage contact lens. if possible. edema and cotton wool infarcts. retina and central nervous system. Open a fresh bottle to avoid intraocular contamination. There may also be bubbles in the anterior chamber. Damage to the iris may result in an irregularly shaped. however. Additional pressure on the globe may result in extrusion of uveal tissue through the wound. as any pressure applied to the globe may cause uveal tissue to extrude through the wound. the patient frequently is lacrimating too heavily for the Seidel test to be performed with any degree of accuracy. exert no pressure upon the eye. it is best not to elevate a patient’s expectations. weakening of the arterioles and capillaries may result in the characteristic appearance of intraretinal dot and blot hemorrhages. vision may improve after surgical repair. In the retina. Seidel’s sign will be present: as fluorescein is added. Fluctuating visual acuity secondary to unstable blood sugar is a common ocular sign. Advise the patient that the initial entering acuity may represent the best vision that the patient can expect to achieve after surgical repair. the less done in the office the better.injury. there will be a flat chamber. Do not unnecessarily manipulate the eye with a full thickness laceration. In these cases. unreactive iris. arrange for the appropriate referral. With a corneal laceration. intraretinal microvascular abnormalities (IRMA) microaneurysms. Proliferative diabetic retinopathy is the result of severe vascular compromise and is visible as neovascularization of the disc (NVD). Instruct the patient to neither eat nor drink prior to the surgical consultation.
produces vascular insufficiency. It is characterized as a disorder of metabolic regulation as a result of deficient or malfunctioning insulin or deficient or malfunctioning cellular insulin receptors. resulting in the vascular leakage of blood. With respect to diabetes. it is not a tool for diagnosis. protein and lipid. regardless of the acuity. In cases where there are large refractive changes. Biochemistry involving the formation of sorbitol plays a role in the destruction of pericytes. capillary endothelium becomes compromised. The formation and release of vasoproliferative factors which play a role in the genesis of retinal neovascularization are poorly understood. fourth and sixth cranial nerves as well as diabetic papillitis and facial nerve paralysis. The Early Treatment of Diabetic Retinopathy Study (ETDRS) has shown that focal/grid laser photocoagulation reduced the risk of moderate vision loss in patients with clinically significant macular edema. which are cells that support the vascular endothelium. As the supportive pericytes perish. 90D Hruby or three-mirror lens). glycosylated hemoglobin or oral glucose tolerance test (OGTT). refer the patient to a retinal specialist. If the patient exhibits either of these high risk characteristics. patients may require a temporary spectacle prescription until the refraction stabilizes. When retinopathy threatens the macula or when new blood vessels proliferate. It identifies the areas of leakage that require focal grid laser photocoagulation. or rubeosis irides). or (3) an area of retinal thickening one disc diameter or greater in size. The most important element of MANAGEMENT is education so that patients are informed that they may eventually need to change their spectacle lenses. either you or the patient's physician should order a fasting blood glucose (FBS). It can only be identified through observation using stereoscopic indirect biomicroscopy (60D. . It defined the high risk characteristics as: (1) Neovascularization of the optic disc (NVD) one-quarter to one-third of a disc diameter in size and (2) Neovascularization elsewhere (NVE) with any vitreous hemorrhage. This. refer him or her to a vitreoretinal specialist. (2) exudate at or within 500 microns of the center of the foveola only if associated with retinal thickening. in combination with thickened. within one disc diameter of the foveola. MANAGEMENT When you suspect ocular sequelae of diabetes mellitus in an undiagnosed individual. Referral is also indicated if you suspect clinically significant macular edema but are having difficulty visualizing the macula or edema. defined as: (1) retinal thickening at or within 500 microns (one-third of a disc diameter) of the center of the foveola. CLINICAL PEARLS • • Clinically significant macular edema is unrelated to acuity and can exist in the presence of 20/20 vision. refer for laser photocoagulation.(NVE) and neovascularization of the iris (NVI. PATHOPHYSIOLOGY Diabetes mellitus is a genetically influenced group of diseases that share glucose intolerance. Fluorescein angiography is only used for treatment. glucose-laden blood. Neurological complications include palsies of the third. If you observe any of these signs. 78D. Most non-vision threatening sequelae of diabetes resolve spontaneously over the course of weeks to months following medical control. The Diabetic Retinopathy Study (DRS) has conclusively proven that panretinal photocoagulation was successful in reducing the risk of severe vision loss in high risk patients. altered structure and decreased function. capillary nonperfusion. retinal hypoxia.
Even in the face of optimal blood sugar control. and the patient is out of immediate danger. as the risk of retinal complications is highest within the six weeks following vitreous detachment. but requires monitoring yearly. As the vitreous detaches peripherally.• Angiography is not required for treating proliferative disease since PRP does not require precise aiming of the laser. If the tear bridges a blood vessel. supported by hyaluronic acid molecules. with detachment of the posterior hyaloid face from the optic disc. a new PVD will present with a small amount of pre-retinal or vitreous hemorrhage without an observable retinal break. This usually is observable ophthalmoscopically as an annulus floating in the vitreous over the posterior pole. POSTERIOR VITREOUS DETACHMENT SIGNS AND SYMPTOMS The patient. areas of vitreoretinal adhesion may result in a tear in the sensory retina with the ensuing possibility of a rhegmatogenous retinal detachment. PATHOPHYSIOLOGY The vitreous is comprised of collagen fibrils and glycoaminoglycans. MANAGEMENT A PVD found asymptomatically on routine examination is benign. If the patient presents with multiple floaters. If no retinal breaks are seen at that point. the blood resulted from torn retinal or disc capillaries. The vitreous may collapse. There is usually one floating spot that is especially large and troublesome to the patient and serves as the impetus to seek immediate care. If no retinal breaks are initially detected. Patients who report diffuse floaters during routine examination usually are suffering from benign vitreous syneresis and not posterior vitreous detachment. There may also be associated photopsia if the patient is experiencing vitreoretinal traction. A patient who presents with a sudden onset PVD without retinal breaks or hemorrhage requires repeat peripheral examination in six weeks. usually over the age of 50. Prophylactically treat any fresh breaks associated with a new PVD immediately with photocoagulation or cryoretinopexy. RETINAL VEIN OCCLUSION . there may be an associated vitreous hemorrhage. routine yearly examination is all that is needed. patients with long-standing disease can be expected to eventually develop some form of retinopathy. This patient needs a detailed peripheral exam using scleral indentation as well as Goldmann and/or Volk lens evaluation. With aging. the patient needs a repeat evaluation every two weeks for six weeks to look for an occult break not originally found. The development of diabetic retinopathy is time-dependent. CLINICAL PEARLS • • Occasionally. If you do not observe any breaks after six weeks. a vitreous hemorrhage ensues. will present with a sudden onset of floaters. especially if there is an associated reduction in visual acuity. reduction in hyaluronic acid causes loss of support to the collagen.
Multiple cotton wool spots indicate retinal ischemia and capillary non-perfusion. . Loss of retinal capillary beds with subsequent retinal non-perfusion will lead to retinal hypoxia and the subsequent release of Non-ischemic Branch Retinal Vein vasoproliferative substance. then the occlusion is considered ischemic. then vision is dramatically and irreversibly lost. cotton wool spots. and may complain of a sudden onset of floating spots or flashing lights. or one of the vein's two Occlusion trunks. vessel anomalies or a combination of these factors. atherosclerosis. Anterior and posterior segment neovascularization may occur later in the disease. with the apex of the hemorrhage at an arteriovenous crossing. and tortuous and Ischemic Central Retinal Vein dilated retinal veins. the closest viable capillary network from which neovascularization will form is typically the posterior iris. This can lead to rubeosis irides and neovascular glaucoma. A hemi-central retinal vein occlusion will involve only the superior or inferior half of the retina. Vasoproliferative factors will then Occlusion stimulate the proliferation of neovascularization from nearby viable capillary beds. In all cases of venous occlusion. there may be a relative afferent pupillary defect. If a significant area of capillary non-perfusion is present. In branch and hemi-central occlusions. disc swelling. if retinal capillary non-perfusion involves the perifoveal region. A branch retinal vein occlusion will present with findings in only one quadrant.SIGNS AND SYMPTOMS The patient will usually be elderly. resulting in perpetual non-perfusion of the retinal tissue. Ophthalmoscopically. The patient may be asymptomatic. but often will complain of sudden painless unilateral loss of vision and/or visual field. the main cause of vision decrease is macular edema. superficial hemorrhages. but may involve abnormal blood flow or blood constituents. as it constricts through the lamina cribrosa. often with a history of systemic diseases such as diabetes and hypertension. This will result in leakage from the capillary beds draining into these vessels. If there is a central retinal vein occlusion. there will be retinal edema. Acuity may range anywhere from 20/20 to finger counting. these Occlusion findings will encompass all four retinal quadrants. neovascularization will most often form on the optic disc or adjacent retina and can lead to vitreous hemorrhage and tractional retinal detachment. PATHOPHYSIOLOGY The etiology of central and hemi-central retinal vein occlusion is an Non-ischemic Hemi-central Retinal Vein obstruction of the central retinal vein. If vision loss is severe. The cause is obscure. The etiology of a branch retinal vein occlusion is an arteriolosclerotic arteriole crossing and constricting the underlying venule. The capillary beds may be irreversibly damaged by this leakage. However. usually supero-temporal. The hemorrhaging may be so severe that all features of the underlying retina are obscured. In central retinal vein occlusions.
disc or retina. and viscosity studies. fundus photography and goniscopy until you see resolution. Monitor the patient monthly with serial ophthalmoscopy. New research indicates that ischemic retinal vein occlusions do not benefit from prophylactic PRP. Central retinal vein occlusion patients with vision reduction due to macular edema do not benefit from the proceudre. Ischemic vein occlusions typically present with acuity worse than 20/200. Those eyes with initial acuity better than 20/200 are at very low risk of developing severe. Due to the association of systemic disease with vein occlusions. sickle dex (if the patient is African-American). according to new research. and they account for only one-third of all occlusions. If the patient has a hemi-central or branch retinal vein occlusion and vision is below 20/40 due to macular edema. It is not indicated initially. the patient will benefit from focal laser photocoagulation anywhere between three and 18 months after the occlusion's onset. then it is likely nonischemic. has questionable use in vein occlusions. comanage the patient with an internist. but later in the disease it will provide information about retinal capillary perfusion and whether or not the occlusion is ischemic and thus more likely to foster neovascularization. complete blood count with differential. permanent vision loss. long held to be the gold standard in assessing retinal vascular disease. lipid and cholesterol studies. withhold this procedure until the patient develops frank neovascularization of the iris. FTA-ABS. Ischemic occlusions are likely to present with a relative afferent pupillary defect. fasting blood glucose. angiotensin converting enzymes. CLINICAL PEARLS • • Ischemic vein occlusions are the only vein occlusions that will likely develop neovascular complications. anti-nuclear antibodies. • RETINAL ARTERY OCCLUSION . as the fresh hemorrhage will block transmission and reveal no useful information.MANAGEMENT Fluorescein angiography. Tests to be ordered include: blood pressure. If not. and are likely to resolve.
Between two and 10 percent of central retinal artery occlusions are caused by thrombus formation from giant cell arteritis (GCA). digital globe massage. The patient often has significant systemic illness such as hypertension and/or diabetes. PATHOPHYSIOLOGY The main cause of retinal arterial occlusions is an embolism lodging in the central retinal artery where it constricts to pass through the lamina cribrosa. If the underlying cause of the central retinal artery occlusion is GCA. Ophthalmoscopically. various methods have been employed to reduce resistance on the artery or dilate the artery to induce the embolus to dislodge. Neovascularization is not common with either central or branch artery occlusions. there will be an area of perfusion from the optic disc to the macula. While there is anecdotal evidence that these measures have sporadically resulted in vision returning. a large study showed that the average final visual outcome in patients with embolic central retinal artery occlusion treated with heroic measures compared to those untreated was only one-quarter line improvement in Snellen acuity. An embolus may be visible in the vasculature on the disc. painless. If a branch retinal artery is involved. unilateral loss of vision and/or visual field. it will do so rapidly. Most practitioners would attempt these measures if the occlusion were less than 24 hours old. cholesterol from an ulcerated carotid artery plaque. The embolism may be comprised of aggregated fibrin and platelets arising from an ulcerated vessel wall thrombus. Abnormal cardiac rhythms may allow blood to coagulate and form emboli which may also reach the retinal vasculature. or in a smaller branch arteriole. but if it does occur. you'll see a pale. or calcium from cardiac valvular disease. edematous retina with attenuated arterioles and a cherry-red macula if the entire central retinal artery is occluded. central retinal artery occlusion has been considered an emergency.Branch Retinal Artery Occlusion Retinal Artery Occlusion SIGNS AND SYMPTOMS The patient. vision could be potentially salvaged with the retina being re-perfused. Acuity may be as low as hand motion. usually between the ages of 50 and 80. It was felt that. if the embolus could be dislodged within 90 minutes of occlusion. there may be a rapid progression to bilateral vision loss if left untreated. will present with a sudden. an embolus will be visible in the vessel with ischemia and infarct appearing distal to the occlusion. If a cilioretinal artery is present. There will be a relative afferent pupillary defect in the involved eye. paracentesis. . milky. To this end. and carbonic anhydrase inhibitors to reduce intraocular pressure and decrease vascular resistance to flow. Common methods employed included breathing into a paper bag to increase blood carbon dioxide levels and induce vasodilation. MANAGEMENT Traditionally. with rubeosis forming approximately four weeks after the occlusion.
Electrodiagnostic testing in RP shows a significantly diminished scotopic ERG as well as an abnormal EOG and dark adaptometry. Most patients with retinitis pigmentosa are myopic. Many patients with RP also experience photopsiae as the disorder progresses. Central retinal artery occlusion may be caused by GCA. Medical testing should include blood pressure evaluation. posterior vitreous detachment and posterior subcapsular cataracts. Color vision is typically remains intact as long as visual acuity is better than 20/40. . These patients are at extreme risk for cardiovascular disease and myocardial infarction. stellate pigment hyperplasia may be noted at perivascular locations in the midperipheral retina. These are believed to represent aberrant electrical impulses from the degenerating retina. lipid and cholesterol levels.g. Central visual acuity is generally not affected until the very late stages of RP. and many patients fail to recognize the manifestations of this condition until it has progressed significantly. atherosclerosis or diabetes. typically they report small flashes of light or a twinkling. like the optic nerve. Later." As the disorder progresses. CLINICAL PEARLS • • • Traditional heroic measures to salvage vision generally do not produce significant changes in the patient's vision. is usually unaffected in the early stages. The onset is often gradual and insidious.. Retinal pigmentary changes occur in the form of fine mottling or granularity with surrounding areas of atrophy. RP has a strong correlation with acquired optic disc drusen. prompt referral to a cardiologist is indicated. Fluorescein angiography is generally not indicated. cystoid macular edema or focal RPE defects. Therefore. bilateral vision loss RETINITIS PIGMENTOSA SIGNS AND SYMPTOMS Patients with retinitis pigmentosa (RP) may present with varying symptoms. although variants have been encountered that cause devastating macular compromise early in the disease course (e. Additional findings in RP include pigment cells in the vitreous ("tobacco dust sign"). When patients do report symptoms.Patients with arterial occlusion have significant systemic illness. fasting blood glucose. The optic nerve head is often normal in early RP. Attenuation of the retinal arterioles is the earliest observable sign in RP. EKG. and hyperviscosity studies. These patients have a significantly reduced survival rate. and many have keratoconus as well. The macula. X-linked recessive RP). These hyperplastic formations are often referred to as "bone spicules. For this reason. but in some forms of RP may demonstrate preretinal gliosis ("cellophane maculopathy"). Patients with central retinal artery occlusion over the age of 60 need an immediate erythrocyte sedimentation rate (ESR) to examine for the possibility of giant cell arteritis. they commonly include difficulty with night vision (nyctalopia) as well as loss of peripheral vision. the patient can develop severe. shimmering sensation in the midperipheral or peripheral field. and the main cause of mortality is cardiac. namely hypertension. but may demonstrate a waxy yellow or pale appearance later. if undetected. these patients need prompt referral to a cardiologist for complete evaluation. general atrophy of the RPE and choriocapillaris ensues. exposing the larger choroidal vessels.
CLINICAL PEARLS • Most patients with RP are diagnosed in the second or third generation of life. which leads to a disturbance in the retinal pigment epithelium (RPE) and the breakdown of the photoreceptors' outer segment disc membranes. age of onset (congenital. retinal gliosis. sectoral. Also stress the potential for visual enhancement through low-vision devices and vision rehabilitation. adult onset). The resultant accumulation of metabolic by-products disrupts retinal function. Implement low-vision services as the disorder begins to affect visual function. multiplex). • • • RETINAL DETACHMENT . Individuals should know the risk for their progeny or other family members developing the disease. resulting in subretinal leakage and macular edema in later stages. particularly in the early stages. and evaluate for cataract or macular edema at least annually. The diagnosis of RP is often based upon appearance. Some presentations are extremely subtle. simplex. Recommend genetic counseling to help the patient deal with these issues. some presentations are atypical. These RPE changes compromise the blood-retina barrier. but many "masqueraders" exist.PATHOPHYSIOLOGY Retinitis pigmentosa is believed to stem from a genetic defect. retinal drug toxicity secondary to thioridazine. or location of retinal involvement (central. Perform visual fields several times a year. Impress upon these patients also that. CMV retinopathy. Understandably. order serology if the diagnosis is unclear or other disorders are suspected. infrared blocking sun lenses and contrast enhancing filters may be helpful. cancer-associated retinopathy. and traumatic retinopathy. photoreceptor loss. syphilitic retinopathy. This is critical to determine the exact inheritance pattern of the patient's condition. There are many forms of retinitis pigmentosa. cone-rod). MANAGEMENT Since there is no known treatment for retinitis pigmentosa. the patient typically experiences visual difficulty under dark conditions. RP may be classified on the basis of inheritance pattern (autosomal dominant. as well as peripheral field constriction. pericentral. management calls for prompt diagnosis and subsequent counseling to maintain quality of life. childhood onset. Periodic optometric follow-up is also important. X-linked. and while most present with similar findings and outcome. toxoplasmosis. the untreatable progressive nature of retinitis pigmentosa is extremely unsettling for the patient and their loved ones. juvenile onset. it is often beneficial to recommend psychological or family counseling early in the disease. Field-expansion devices. although they cannot be cured. and manifests as lipofuscin deposition. Because of the insidious nature of the disorder. including rubella retinopathy. Always obtain visual fields and electrodiagnostic testing to confirm the diagnosis of RP. pigmented paravenous retinochoroidal atrophy. peripheral). the earliest indicators are often objective findings rather than subjective complaints. choriocapillaris occlusion and RPE hyperplasia. chlorpromazine or chloroquine. they still require periodic examination to assess their status as well as manage their ongoing refractive needs. predominant photoreceptor involvement (rod-cone. Because the affected photoreceptor cells in most cases are rods. autosomal recessive. Most experts recommend a pedigree analysis of patients once RP has been diagnosed. Perform a critical evaluation on all patients presenting with complaints of nyctalopia or peripheral field loss.
ERD appears clinically as a focal. dome-shaped protrusion of the retina. however it may shift and then return to its original orientation with quick eye movements. this fluid is liquefied vitreous. It is sometimes difficult to assess where the necrotic retina ends and the vitreal membranes begin.SIGNS AND SYMPTOMS There are three forms of retinal detachment: 1. peripheral visual field loss. Very often. which results from a retinal break. Exudative detachments do not generally present with photopsiae but may be associated with moderate vision loss. Tractional retinal detachment (TRD). Exudative or serous retinal detachment (ERD). with patients reporting photopsiae. These may result from preexisting conditions or ocular trauma. resulting in a retinal "pseudo-hole. In cases of extensive unilateral retinal detachment. lackluster appearance with undulating retinal folds. A rhegmatogenous detachment will not change position with changes in body posture. you may note a milky. Retinal pigment epithelial hyperplasia may be noted in cases of long-standing retinal detachment (pigment demarcation line). Intraocular pressure may be reduced in eyes with acute retinal detachment. in which case the patient can suffer severe and abrupt vision loss. which shifts position with changes in posture and eye movement. 3. Ophthalmoscopy in cases of RRD usually reveals a clumping of pigment cells within the anterior vitreous (Shaffer's sign). If a significant area of the retina is involved. you may observe a relative afferent pupillary defect. TRD is always associated with vitreal strands and membranes. The vast majority of rhegmatogenous detachments are symptomatic. PATHOPHYSIOLOGY All retinal detachments involve the sensory retina dissecting from the underlying pigment epithelial layer by subretinal fluid. Tractional detachments are typically asymptomatic unless central vision is threatened. translucent. Both passive and active movement of subretinal fluid induce progression of retinal detachments. and is a good prognostic feature. Retinal breaks are the predisposing factor in patients with rhegmatogenous detachment. serous elevation of the retina. The subretinal fluid obeys gravity. central blurring of vision or metamorphopsia. There are usually no hemorrhages. Associated findings may include posterior vitreous detachment and preretinal or vitreal hemorrhage. In rhegmatogenous detachments. the fluid is derived from the choroid. In exudative detachments. this area encircles an intact posterior pole." TRDs are dense and immobile. which results from the pull of proliferative fibrovascular vitreal strands. metamorphopsia or a visual field deficit. except in cases of associated retinal vasculopathy. Rhegmatogenous retinal detachment (RRD). Some of the more common entities associated with RRD . 2. which results from fluid accumulation under the sensory retina without a retinal break. which accesses the subretinal space via a retinal break. smooth-surfaced detachment with marginal fibrovascular bands emanating into the vitreous body. This motility lends itself well to ancillary testing with ultrasonography. The origin of the subretinal fluid in tractional detachments is unknown. leading to partial or total loss of vision in some patients. It appears as a concave. There may be an area of white or grayish elevated retina adjacent to the instigating retinal break. passing through a defective Bruch's membrane. floating spots. always affecting the lowest aspect of the eye. Ophthalmoscopy reveals a smooth.
Without surgical intervention. however the former has fewer applications and is therefore done less frequently. death of this tissue occurs within 48 to 72 hours. (Silicone oil tamponade was actually used prior to the advent of pneumatic retinopexy. on the other hand. and acquired retinoschisis with both inner and outer holes. the involved portion of the retina changes.) Silicone oil tamponade is most commonly used to repair RRD resulting from cytomegalovirus infection in AIDS. the traditional surgery for retinal detachment. Vogt-Koyanagi-Harada syndrome. chronic or long-standing RRDs requiring treatment should be addressed within one week of diagnosis.). Treatment options for RRD include scleral buckling procedures. . under general anesthesia. Transudation of fluid through the RPE defects causes detachment of the otherwise normal sensory retina. operculated retinal breaks. is more common for treating smaller. Most practitioners are familiar with scleral buckling procedures. Coat's disease and uveal effusion syndrome. pneumatic retinopexy and intraocular silicone oil tamponade. true retinal detachments require surgical repair. This explant is sutured into place to reestablish adhesion between the sensory retina and RPE. The most common of these is proliferative diabetic retinopathy. Unlike rhegmatogenous or exudative detachments which tend to be abrupt. Macular TRDs. Exudative detachments are relatively rare. congenital optic disc anomalies (optic pits. Peripheral TRDs are therefore rarely if ever noticed by the patient. progressing at the same rate as the associated fibrovascular proliferation. an intravitreal gas bubble (usually perfluoropropane. flap tears. atrophic holes. and the subretinal fluid is drained via a small scleral incision. All other fresh RRDs should be repaired within 24 to 48 hours. posterior scleritis. a soft silicone sponge or hard silicone band is used to indent the eye at the point of detachment. In pneumatic retinopexy. In certain instances. or to encircle the eye if the detachment is significant. occurring in association with subretinal disorders that damage the RPE layer. The retinal tear is first repaired with cryopexy. tend to be symptomatic. As the retinal tissue loses its connection to the RPE. As the fluid shifts with eye and head movements. etc. Careful eye and head positioning are important postoperatively to ensure resolution. Cryopexy is performed at the site of the break. morning glory syndrome. silicone oil tamponade may be favorable to either of these techniques. it becomes edematous and dysfunctional. superiorly located detachments. and then the gas is injected into the vitreal cavity. This explains why most patients with ERDs suffer significantly less devastating visual compromise than those with RRDs or TRDs. sickle cell retinopathy.include lattice degeneration. The etiology of TRD involves fibrotic scaffolding of the vitreous along proliferative vascular networks which induce strong anterior tractional forces through vitreal shrinkage. These may include choroidal neoplasms. This procedure is identical to pneumatic retinopexy except that silicone oil replaces the expansive gas. These forces induce the sensory retina to separate from the underlying RPE. This technique. MANAGEMENT Patients presenting with an acute onset rhegmatogenous detachment that involves or threatens the macula warrant immediate retinal specialist consultation. performed under local anesthesia. TRDs are often slow and insidious. unless the underlying disease process has already compromised visual acuity. Tractional detachments occur only in proliferative vitreoretinopathies. but many TRDs are associated with ischemic retinal vein occlusions. toxocariasis and trauma. While small retinal breaks or atrophic holes may be managed with laser photocoagulation or cryopexy. Then. C3F8) serves to reattach the retina. retinopathy of prematurity.
This may involve high-dose steroids in the case of inflammatory disorders. Surgical repair of TRD usually involves pars plana vitrectomy.) must undergo a thorough dilated fundus evaluation. you faced a dilemma. etc. knowing full well that the patient might never develop a problem from the elevated IOP. OHTS also attempted to identify which patients would most likely benefit from treatment. Conservative surgical management may still be indicated for partial or sectoral RRDs. While race (blacks) and family history were expected to be . superior detachments present a greater urgency than do other RRDs. • • • New Insights Into Treating Ocular Hypertension In the past. On one hand.5% to 4. Refer fresh rhegmatogenous detachments immediately for evaluation and surgical intervention. Perhaps the visual field defect that developed would be a troublesome paracentral scotoma. or radiation therapy and/or local resection in the case of intraocular neoplasms. Tractional detachments represent the most ominous sequela of proliferative vitreoretinopathies. with scleral indentation where appropriate. For this reason. blunt ocular trauma. you could watch for glaucomatous change before initiating therapy. proliferative diabetic vitreoretinopathy. This year we saw the publication of The Ocular Hypertension Treatment Study (OHTS) results and its companion piece. intervention is often not attempted unless the macula is involved or threatened. although many practitioners erroneously believe so).2 There were some surprising results. require intervention less often than do RRDs. In cases of long-standing retinal detachment. you could initiate IOP reduction therapy.Exudative detachments.1 Thus. make patients aware of the permanent nature of the vision loss. CLINICAL PEARLS • Failure to diagnose retinal detachment remains the second-most-common malpractice claim against optometrists. or the initial damage might make the remaining fibers more susceptible to further damage. ERDs will usually resolve spontaneously with appropriate management of the underlying condition. because of their nature. and are often related to more severe conditions that may need to be co-managed with an ophthalmologist. it is also easy to see that initiating therapy on every patient with ocular hypertension would result in gross over-treatment. Because of their progressive nature. as the potential risks outweigh the benefits. Again. tractional detachments are typically more difficult to manage than either RRDs or ERDs. Complete RRDs lasting more than two weeks are usually not treated surgically. This study has greatly increased our understanding of ocular hypertension and the risk for developing glaucoma. because of the forces of gravity (this rule does not apply to retinal breaks without detachment. to secure the remaining retina against the odd chance of ocular trauma and subsequent detachment. knowing that 20% to 50% of the optic nerve fibers may be lost before you could make a conclusive diagnosis. Exudative retinal detachments are encountered far less frequently than RRDs. IOP reduction in ocular hypertension did benefit some patients. On the other hand. Notably. particularly if the macula is involved or threatened.4%. In addition. Silicone oil tamponade is another popular technique for the treatment of tractional detachments. However. when a patient's intraocular pressure (IOP) was elevated with normal visual fields and optic nerves. and would be incurring the expense and risks associated with therapy. All patients presenting with symptoms of retinal detachment or a predisposing history (peripheral retinal thinning or breaks. the study concluded that lowering IOP in patients with ocular hypertension reduced the risk of developing glaucoma in five years from 9. ongoing ophthalmologic co-management should be the rule in these cases.
Surprisingly. However. older age. Central corneal thickness appears to be a powerful predictor of the progression from ocular hypertension to POAG.predictive of the development of POAG. . Not unexpectedly. though other unknown factors may contribute to this finding. and higher IOP were predictive of glaucoma. The study shows patients with thin central corneas are likely to benefit most from IOP reduction. they weren't strongly predictive. The theory holds that the rigidity of a thick cornea artificially elevates the Goldmann applanation measurement of IOP and a thin cornea consequently lowers the reading of the true IOP. Rarely are the conclusions of a landmark study so emphatic: At this time. measurement of central corneal thickness is necessary to accurately manage patients with ocular hypertension. larger initial cup-to-disc ratio. Patients with a central corneal thickness of 555µm or less had a three-fold greater risk of developing POAG than those with a central corneal thickness of 588µm or greater. the presence of diabetes seemed to protect patients from the development of glaucoma. the factor that was most predictive was the presence of a thin central cornea.
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