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Monday, October 31, 2011

UVEITIC GLAUCOMA & GLAUCOMATOCYCLITIC CRISIS  

SIGNS AND SYMPTOMS
Patients with uveitic glaucoma will present with a unilateral red, painful, photophobic, lacrimating eye. Acuity will be moderately decreased. There will be corneal edema and folds in Descemet's membrane, but the epithelium should be intact. There will be a profuse anterior chamber reaction, possibly with hypopyon. There are frequently posterior synechiae. There will be injection of the conjunctival and episcleral vessels. The angle may be closed with peripheral anterior synechiae (PAS). Intraocular pressure (IOP) may range from 30 to 80mm Hg.

The patient with glaucomatocyclitic crisis will present with a recurrent, unilateral red eye with very mild discomfort, or possibly no discomfort at all. Acuity will be mildly reduced; this is often the chief complaint. The cornea will be mildly edematous, but the anterior chamber will be remarkably clear. Often, the only signs of anterior chamber inflammation will be a rare cell or two in the chamber or, more commonly, a few keratic precipitates on the endothelium. Intraocular pressure can range from 30 to 70mm Hg, but the patient will not be in acute distress.

PATHOPHYSIOLOGY
In uveitic glaucoma the patient first develops uveitis, either due to trauma, systemic disease or idiopathically. The ensuing inflammation results in a rise in IOP through several mechanisms.

Often, the inflammatory cells physically block the trabecular meshwork, decreasing aqueous outflow, with the angle remaining open. Occasionally, the inflammatory cells and fibrous protein will form a connective bridge between the peripheral iris and cornea, pulling these structures into apposition, and resulting in an angle closure with PAS formation.

Because the inflammatory cells and protein in the anterior chamber form adhesions between the posterior iris and anterior lens, posterior synechiae commonly form. This will lead to iris bombé, secondary angle closure and peripheral anterior synechiae formation. There may also be a combination of mechanisms that increases IOP. Untreated, the patient will eventually experience glaucomatous optic atrophy, or possibly central retinal artery occlusion.

In glaucomatocyclitic crisis, there is an idiopathic inflammation of the trabecular meshwork that reduces this structure's ability to actively drain aqueous. Due to prostaglandin release, it is theorized that there may also be a concurrent overproduction of aqueous. Despite the elevated IOP, this condition is only mildly symptomatic, and is usually self-limiting. However, the recurrent nature of the attacks predisposes the patient to developing glaucomatous optic atrophy.

MANAGEMENT
Successful management of uveitic glaucoma involves prompt and aggressive measures. In any inflammatory glaucoma, you must treat the inflammation first and the IOP secondarily. Initiate strong cycloplegia in the form of atropine 1% BID immediately to put the uveal tissue at rest and begin healing. Have the patient use a steroid such as Vexol (rimexolone), Pred Forte (prednisolone acetate) or fluorometholone acetate (Flarex, Eflone) every 15 minutes for the first several hours, then taper to every hour.

If any posterior synechiae have formed, prescribe phenylephrine 10% BID. Quelling the inflammation will temporize the IOP rise. To further reduce the IOP, use a topical beta-blocker BID or the topical carbonic anhydrase inhibitor Trusopt TID, provided there are no medical contraindications to any of these drugs. Avoid pilocarpine and other miotics in these patients. Follow the patient every 24 hours and gradually taper the medications as the condition improves.

Management of glaucomatocyclitic crisis is nearly identical to that described above for uveitic glaucoma, with the following two exceptions:

(1) It is acceptable to use a slightly weaker cycloplegic such as scopolamine (hyoscine 0.25%) or homatropine 5% BID.

(2) The patient should instill a topical steroid hourly rather than every 15 minutes.

CLINICAL PEARLS

Avoid pilocarpine and other miotics in inflammatory glaucoma. Miotics will induce ciliary spasm and increase inflammation, fostering both posterior and peripheral anterior synechiae. We have seen many cases of inflammatory glaucoma improperly treated with pilocarpine; all patients worsened considerably and one ultimately resulted in enucleation.

Steroids are absolutely necessary to manage inflammatory glaucoma. However, practitioners tend to be hesitant to prescribe steroids for patients with elevated IOP for fear of a concomitant steroid-induced pressure rise. One must realize that steroids will not increase IOP for at least two weeks, and this pressure rise only occurs in one-third of the population. In fact, steroids will actually reduce IOP by quelling the inflammation. Withholding steroids in inflammatory glaucoma is extreme mismanagement.

Strong cycloplegia is necessary in managing uveitic glaucoma. The use of tropicamide, cyclogel or other weak cycloplegic agents is considered poor management.

Avoid the prostaglandin analog latanoprost (Xalatan) since, as in any inflammatory condition, there will already be copious amounts of prostaglandins in the anterior chamber and Xalatan will not provide any benefit.

Remember: treat the inflammation first and the IOP secondarily!

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.

PATHOPHYSIOLOGY
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.

MANAGEMENT
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.

CLINICAL PEARLS
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.")

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.

PATHOPHYSIOLOGY
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.

MANAGEMENT
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.

CLINICAL PEARLS
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.")

Fuchs’ Endothelial Dystrophy

Signs and Symptoms
Late hereditary (Fuchs’) endothelial dystrophy is usually seen in the fifth or sixth decade of life. It is more common in women than men, bilateral, and usually of dominant inheritance. The dystrophy itself stems from the primary malfunction of the corneal endothelium. This ultimately causes the disruption of the corneal dehydration system and consequently a physiologically and optically compromised tissue. Presenting symptoms include decreased vision, foreign body sensation and pain upon waking. Biomicroscopic findings include focal thickenings of the Descemet’s membrane known as corneal guttata, corneal stromal edema, folds in Descemet’s membrane secondary to corneal edema, fine pigment dusting on the corneal endothelium, and in advanced stages, corneal pannus, and bullous keratopathy. In general, corneal dystrophies exhibit familial patterns and have no association with systemic or environmental factors. It is associated with a slightly increased prevalence of open angle glaucoma.

 


Pathophysiology
The cornea consists of five discrete layers: epithelium, Bowman’s layer, stroma, Descemet’s membrane and endothelium. When healthy, the endothelial cell layer is a single stratum of hexagonal cells that borders Descemet’s membrane. It shows great metabolic activity and is actively involved in the maintenance of corneal dehydration. Following trauma or injury, the surrounding endothelial cells slide over to the injured area. There is no mitotic activity in the adult endothelium. This focal enlargement and/or change in shape of the endothelial layers can be seen using special biomicroscopic techniques and is called polymegathism and pleomorphism, respectively.

The clinical and histopathological progression of Fuchs’ is complex, but can best be divided into three stages, which usually span 10 to 20 years. In the first stage the patient is initially asymptomatic, but manifests central irregularly distributed guttata warts and geographically arranged pigment dusting. Occasionally, a diffuse brown pigmentation of the central posterior surface is also seen. Histologically, the endothelial cells show degeneration and deposition of abnormal Descemet’s membrane material.

In the second stage the patient develops stromal and epithelial edema, with symptoms of glare and hazy vision. Visual acuity is usually 20/30 or better. As edema increases, the stroma thickens centrally, the opacity spreads peripherally and the epithelium develops bullae, which correspond to intraepithelial lakes of fluid. As stromal edema increases, Descemet’s membrane develops folds and vision falls. Eventually, the benefit of better vision late in the day is lost, the epithelium becomes more bullous, and pain and photophobia develops.

In the third phase, subepithelial connective tissues appears centrally. This is an avascular tissue that does not migrate in from the periphery like pannus, but arises in the central cornea. Clinically, it appears as an irregular, dense, gray, swirling sheet of scar tissue. Histologically, it consists of active fibroblasts and of large and small collagen fibrils between Bowman’s layer and the epithelium. In advanced cases, the stromal edema and epithelial bullae disappear as the stroma scars, and the patient becomes more comfortable even though the visual acuity is severely reduced.

Management
The treatment for Fuchs’ endothelial dystrophy varies, depending upon the severity of the disease, and may range from hypertonic drops to surgical intervention. Patients with early stromal and/or epithelial edema may be treated conservatively at first with 5% sodium chloride drops q.i.d. and 5% sodium chloride ointment at bedtime. (Use of a hair dryer held at arms length from the surface of the cornea, in combination with the hyperosmotic agents, may dry out the corneal surfaces and decrease the time the blur persists.)

A therapeutic soft lens (bandage lens) is beneficial in alleviating patient discomfort. A loosely fitting, flat, high-water content soft contact lens will decrease the irregular astigmatism and the pain from ruptured epithelial bullae. This mode of treatment has made life more pleasant for patients who could not afford corneal transplants or who are awaiting a triple procedure with advancing cataract. Take note that any elevation of IOP forces more fluid into the stroma across the compromised endothelium. Appropriate pressure reduction with topical and or oral ocular antihypertensive medications may decrease the progression and symptoms secondary to corneal edema. Corneal grafts for Fuchs’ dystrophy account for approximately 10 percent of all corneal grafts performed. Generally, if the graft is performed before there is involvement of the peripheral cornea, there is an 80 percent likelihood that the graft will remain clear for two years. Keratoplasty in eyes with narrow angles should include lens removal to avoid angle closure with formation of peripheral anterior synechiae. Patients with both Fuchs’ endothelial dystrophy and cataracts will do well with a combined penetrating keratoplasty and cataract extraction.

Clinical Pearls

Corneal guttata seen in young, asymptomatic patients are known as Hassall-Henle bodies and are of no clinical significance.

Excessive central guttata in the absence of corneal edema is termed endothelial cell dystrophy. Endothelial cell dystrophy may remain stable or progress to Fuchs’ dystrophy.

Salzmann’s Nodular Degeneration

Signs and Symptoms
Most cases of Salzmann’s nodular degeneration present asymptomatically. Discomfort does not usually occur until later stages, at which time recurrent corneal erosion (RCE) may ensue. Patients manifesting RCE typically report photophobia, blepharospasm, tearing, and decreased acuity. In between bouts of RCE, non-specific "dry eye" complaints such as burning or grittiness are typical.

Clinically, Salzmann’s degeneration appears as an accumulation of bluish-white superficial nodules in the mid-peripheral cornea. Generally, the eye is not inflamed unless there is associated corneal erosion. In that event, there will be limbal injection, corneal edema, and an anterior chamber reaction.

There are conflicting reports regarding the laterality of Salzmann’s degeneration; an older study reports a unilateral presentation in 80 percent of cases, while a more recent study suggests a bilateral predilection in 80 percent. The condition is seen more frequently in women than in men.

Patients with Salzmann’s degeneration usually describe a previous episode of ocular inflammation, often in childhood. Associated disorders may include phlyctenular disease, vernal keratoconjunctivitis, trachoma, or interstitial keratitis. Patients with a history of epithelial basement membrane dystrophy or corneal surgery may also be at increased risk.

Pathophysiology
At the cellular level, the nodules seen in Salzmann’s degeneration represent clumped masses of collagen fibrils anterior to Bowman’s membrane. Experts speculate that these peripheral accumulations of collagen are produced by fibroblasts within the conjunctiva or limbal vessels. In some cases, transmission electron microscopy has demonstrated reduplication of the epithelial basement membrane. Descemet’s membrane and the corneal endothelium are characteristically unaltered, however.

One theory behind the development of Salzmann’s degeneration suggests that the inciting corneal inflammation creates an irregular surface, allowing for uneven tear film distribution and exposure. A process known as hyalization ensues, which is the same process responsible for the development of conjunctival pinguecula. As the nodules grow in size, there is progressive damage and scarring at the level of Bowman’s membrane. This ultimately results in epithelial erosion and potential impairment of acuity.

Management
Mildly asymptomatic cases of Salzmann’s degeneration may be managed with topical lubricants and/or a bandage contact lens. Prophylactic antibiosis is advisable if epithelial defects are significant. In more severe cases, superficial keratectomy may be utilized to remove the nodules from the anterior cornea. Phototherapeutic keratectomy (PTK) is also an option. If significant scarring is present, or if chronic epithelial breakdown makes the condition unmanageable, lamellar or penetrating keratoplasty may be the only recourse.

Clinical Pearls

The critical issue in managing Salzmann’s degeneration is proper diagnosis. Conditions such as band keratopathy, spheroid degeneration (climatic droplet keratopathy), and corneal keloids may all present with a similar clinical appearance. Consult a corneal specialist in those cases where diagnosis is elusive.

It may be tempting to use topical corticosteroids in Salzmann’s degeneration, particularly if the patient is symptomatic. However, since this condition is non-inflammatory in nature, steroids will have little effect. Additionally, the use of steroids introduces an unnecessary risk in patients with a compromised epithelium.

CORNEAL LACERATION

Signs and Symptoms
The patient with a corneal laceration has experienced significant ocular trauma, typically from a metallic object such as a hand tool. (Fingernail scratches, for example, do not usually have enough force to lacerate a cornea.) There is intense pain initially which may diminish slightly due to corneal desensitization. Patients are photophobic and lacrimate profusely. There is a significant attendant uveitis and the anterior chamber is shallow or even flat in a full thickness laceration. Intraocular pressure generally ranges from 2 to 6 mmHg. Bubbles within the anterior chamber are a key finding. There is significantly reduced visual acuity. Other associated findings may include lens dislocation, iridodialysis, and hyphema.

Pathophysiology
A corneal laceration results from direct trauma to the cornea, typically from a metallic object impacting with sufficient force. There may be either a full thickness laceration or a partial thickness laceration. A full thickness laceration is termed a penetrating injury. In full thickness lacerations, there will be a flat chamber. Seidel’s sign will be present: as fluorescein is added, you will see the aqueous oozing out from the wound amidst the fluorescein. There may also be bubbles in the anterior chamber. Damage to the iris may result in an irregularly shaped, unreactive iris. Additional pressure on the globe may result in extrusion of uveal tissue through the wound.

Management
The diagnosis of corneal laceration must be made as quickly as possible with as little intervention as possible. Additionally, a partial thickness laceration must be differentiated from a full thickness laceration with the use of Seidel’s test. Intraocular pressure measurement should be avoided in any cases suspected to be full thickness lacerations, as any pressure applied to the globe may cause uveal tissue to extrude through the wound. Visual acuity must be taken, if possible. Judicious use of a topical anesthetic will alleviate patient discomfort and allow the clinician to make an appropriate diagnosis. Open a fresh bottle to avoid intraocular contamination.

Do not unnecessarily manipulate the eye with a full thickness laceration. A topical antibiotic solution may be judiciously applied. Absolutely avoid pressure patch or bandage contact lens. Use an eye shield to protect the eye. Again, exert no pressure upon the eye. Arrange for the corneal laceration to be surgically repaired by a corneal specialist immediately. Instruct the patient to neither eat nor drink prior to the surgical consultation.

Clinical Pearl

With full thickness corneal lacerations, the less done in the office the better. Assess the injury, arrange for the appropriate referral, and shield the eye gently for protection while the patient is in transit to the surgeon.

With a corneal laceration, the patient frequently is lacrimating too heavily for the Seidel test to be performed with any degree of accuracy. In these cases, a shallow or flat anterior chamber or the presence of bubbles within the anterior chamber indicates a breach in the corneal integrity.

Advise the patient that the initial entering acuity may represent the best vision that the patient can expect to achieve after surgical repair. Of course, vision may improve after surgical repair; however, it is best not to elevate a patient’s expectations.

Thygeson's Superficial Punctate Keratopathy

SIGNS AND SYMPTOMS
The signs and symptoms of Thygeson's superficial punctate keratopathy (SPK) are minimal. Patients usually report only a mild to moderate foreign body sensation, tearing and occasionally photophobia. There is no history of recent ocular inflammation, nor typically any associated systemic illness. Upon gross inspection, the affected eye appears normal, with little or no evidence of eyelid swelling, conjunctival injection or corneal edema.

Biomicroscopy reveals numerous round or stellate areas of coarse, gray, slightly elevated intraepithelial opacities. These lesions resemble subepithelial infiltrates, but are more superficial, duller in color, and less organized. Also, these areas may demonstrate variable central staining with sodium fluorescein, whereas subepithelial infiltrates typically do not stain. Inspection of the anterior chamber shows neither cells nor flare.

Visual acuity may be normal or mildly reduced, depending upon the density and location of the opacities. Because Thygeson's SPK tends to run a chronic, remittent course, the patient may report similar experiences in the past. The clinical presentation, although bilateral in nature, may be asymmetric, or involve only one eye at a time.

PATHOPHYSIOLOGY
The etiology of Thygeson's SPK is unknown. Research indicates, however, that the condition may be caused by a chronic subclinical viral infection affecting the deeper layers of the corneal basal epithelium. The opacities represent corneal mononuclear cell infiltrates consistent with a viral entity. Studies have implicated a varicella virus, possibly herpes zoster, as well as Chlamydia trachomatis in the development of Thygeson's, although these claims are unsubstantiated.

In most cases, Thygeson's SPK presents with insidious onset. With or without treatment, the lesions will eventually resolve; however, the disease often continues to plague these patients for months or even years, with sporadic exacerbations. The trigger mechanism for these flare-ups appears to be idiopathic.

MANAGEMENT
Thygeson's SPK is a self-limiting disorder, but intervention usually speeds the resolution and enhances patient comfort. Manage mild cases by recommending non-preserved artificial tear preparations, every two to three hours while awake, with bland ophthalmic ointment at bedtime.

Treat more severe presentations with topical steroids, such as 0.1% fluorometholone alcohol (FML) or 1% rimexolone (Vexol). In most cases, QID dosing is adequate, but increase dosage in severe cases if necessary. Continue the treatment for one week, and then slowly taper therapy to avoid a rebound inflammation. Follow up weekly during therapy, then every three to 12 months during remission.

CLINICAL PEARLS

Thygeson's SPK is enigmatic; it presents as a corneal inflammation associated with an essentially white and quiet eye in an otherwise healthy patient. Other conditions that present with corneal infiltrates usually induce at least a related conjunctivitis-the most common of these is epidemic keratoconjunctivitis. Other entities in the differential include: bacterial keratoconjunctivitis, chlamydial keratoconjunctivitis, toxic keratoconjunctivitis, exposure keratopathy and dry eye syndrome.

Because of the chronic, remittent course of this disease, patients often present with their diagnosis "in hand." Patients who are not already aware should be educated about the recurrent nature of Thygeson's SPK, and the need for continued follow-up.

Epithelial Basement Membrane Dystrophy (EBMD)

SIGNS AND SYMPTOMS
EBMDs are bilateral, often asymmetrical corneal basement membrane disorders usually occurring in individuals over 30. Symptoms vary, ranging from nothing at all to mild, short-lived corneal irritation upon waking with photophobia or glare.

Approximately 10 percent of affected individuals develop transient blurred vision with painful recurrent epithelial erosions. Most patients experience fluctuating visual acuity without discomfort. Signs of EBMD include corneal epithelial microcysts, whorling defects known as "fingerprints" or "mare's tails," and positive and negative sodium fluorescein staining.


PATHOPHYSIOLOGY
A dystrophy is a non-infectious, non-inflammatory defect secondary to malnutrition or faulty metabolism. There are four principle classes of corneal dystrophies:

anterior dystrophies
dystrophies of Bowman's layer
stromal dystrophies
endothelial dystrophies

Anterior EBMDs are variants of one cardinal pathophysiology. They are diagnosed and named principally by their appearance. In EBMD disorders, the basal epithelial cells manufacture abnormal finger-like projections that protrude from the abnormally thickened basement membrane. These projections reduce adherence of the overlying epithelium, and produce the characteristic changes. Fibrogranular ridges associated with, and adjacent to, these extensions form the fingerprint patterns. These protuberances bend in the epithelium, trapping cells and intercellular debris to mold microcysts. When a series of microcysts become grouped together and migrate forward, corneal surface abnormalities and RCE occur.

MANAGEMENT
The corneal changes of EBMD patients can be monitored closely with keratometry (paying specific attention to mire quality) and biomicroscopy. Carefully assess the tear film and wetting stability of the corneal surface to determine if keratitis sicca is present.

As opposed to the end of day symptoms of dry eye, the symptoms of EBMD are most severe in the morning. Sodium fluorescein staining reveals surface irregularities and illuminates areas of positive staining (bright green: missing epithelium) and negative staining (free of fluorescein: heaped epithelium). As an option, use rose bengal or lissamine green to reveal areas of devitalized corneal cells.

Treat asymptomatic patients with prophylactic supportive therapies. Artificial tear drops QID PRN, ointments HS-TID, punctal plugs, blindfolds during sleep and goggles or spectacles that prevent dust exposure and add ocular moisture retention support are helpful. Moderate presentations may require hypertonic drops and ointments (NaCl 5%), Q3H to QID, for a minimum of six months. You can prescribe soft contact lenses to smooth surface disturbances when intolerable levels of acuity exist in severe presentations.

Patients with acute recurrent corneal erosion may require debridement of the loose epithelium, topical cycloplegia (cyclopentolate 1% TID or homatropine 5% BID), topical prophylactic antibiotic drops QID (tobramycin, ofloxacin), or ointments and topical hypertonic drops and/or ointment. Manage pain with cold compresses, oral analgesics or topical nonsteroidal anti-inflammatory preparations (Voltaren, BID to QID, or Acular, BID to QID).

The long-term management of RCE follows the same course as EBMD. Cases of RCE that resist medical management may require surgical procedures. Anterior stromal puncture (ASP) under topical anesthesia involves the use of a 25g needle to place 0.1mm deep perforations, breaching Bowmans's membrane, at 0.25mm intervals in a chronic RCE zone in an attempt to initiate scar formation and healing. ASP can also be achieved using the Nd:Yag laser. Dispense appropriate topical cycloplegic, antibiotic, steroidal and hypertonic medications following the procedure. Pressure patching is also an option. Excimer photorefractive therapeutic keratectomy (PTK) to smooth the corneal surface is an effective alternative modality.

CLINICAL PEARLS

The use of the pressure patch remains controversial. While it is still considered acceptable, many clinicians are electing not to patch, citing inability to medicate topically and inconvenience to the patient. While contact lenses may be valuable for smoothing corneal surface irregularities, many practitioners avoid them as bandage devices to keep therapy simple.

There is no evidence suggesting topical nonsteroidal anti-inflammatory medicines increase healing time.

Since many sources suggest an autosomal dominant inheritance pattern, clinicians should closely examine the family members of any EBMD patient.

Chemical Burns

SIGNS AND SYMPTOMS
The diagnosis of chemical trauma to the eye is typically based upon the history, rather than the signs and symptoms. Patients generally report varying degrees of pain, photophobia, reduced vision, and colored haloes around lights.

In mild to moderate burns, the eye is hyperemic and may display conjunctival chemosis, eyelid edema, first degree burns to the skin, and cells and flare in the anterior chamber. Corneal findings may range from diffuse superficial punctate keratopathy to focal epithelial erosion with mild stromal haze.

When the chemical injury is severe, the eye is not red but appears white due to ischemia of the conjunctival vessels. Chemosis of the lids and conjunctiva is evident, and surrounding facial areas may demonstrate second or third degree burns. Corneal findings include total epithelial erosion with edema and dense stromal hazing, and sometimes complete opacification.

PATHOPHYSIOLOGY
Both acidic (pH<4) and alkaline (pH>10) solutions are capable of inducing a chemical burn. Acids tend to bind with tissue proteins and coagulate the surface epithelium. This bars further penetration so acid burns are typically confined to superficial tissues. Most commonly, acid burns to the eye result from exploded car batteries, which contain sulfuric acid.

Alkaline burns occur more frequently and are generally more severe than acid burns. These solutions destroy the cell structure not only of the epithelium but also of the stroma and endothelium. While acids create an initial burn and then cease, alkalis may continue to penetrate the cornea long after the initial trauma. Common sources of alkalis include ammonia, lye and lime.

MANAGEMENT
A chemical burn requires immediate care. The patient needs prompt, copious fluid irrigation of the affected eye, particularly with alkaline trauma. If the initial contact with the patient is by telephone, advise flushing the eye with water for twenty to thirty minutes before coming to the office or clinic. If a patient presents without having irrigated the eye, perform a prolonged lavage with saline solution before any other procedures.

Next, test the eye with litmus paper to establish the residual pH. If near neutral (i.e. 6 to 8), the lavage may be discontinued. Check the lids and fornices and remove any particulate matter (more common with drain cleaners, cement, etc.). Debride any necrotic corneal or conjunctival tissue under the biomicroscope, using a cotton-tipped applicator moistened with antibiotic solution; swab the fornices in a similar fashion. Following this, a strong cycloplegic agent (e.g. 0.25% scopolamine) and broad spectrum antibiotic ointment should be instilled.

If significant epithelial erosion has occurred, consider a pressure patch. In cases of very severe burns, the patient may need to use a topical corticosteroid judiciously during the first week following trauma (1% prednisolone acetate Q2-4H). Depending upon the level of pain, a narcotic analgesic may also be necessary. Evaluate patients daily, and continue medications until resolved. It is also important to monitor the intraocular pressure; IOP spikes may occur as late complications of chemical burns due to blockage of the trabecular meshwork by inflammatory debris.

CLINICAL PEARLS

The most important consideration in chemical burns is immediate irrigation. This single measure offers the best chance of reducing the ultimate physical damage to the eye.

Know your "comfort zone." Don't hesitate to refer to a corneal specialist.

Most acid burns are manageable if they present with mild to moderate stromal haze-they will only get better with time. Alkaline burns, on the other hand, may require some thought, as the presentation at day one may be far better than that seen at day two or three. If there is significant necrosis and perilimbal ischemia at presentation, and if the cornea is even moderately hazy, consider referring the patient as soon as the immediate condition is stabilize.

Blow-out Fracture

SIGNS AND SYMPTOMS
Patients manifesting orbital blow-out fracture always present with a history of blunt ocular trauma. Blow-out fracture is usually caused by a large, low-velocity object, such as a fist or a ball. Sports-related injuries are common. If the trauma is recent, the patient may present with symptoms of pain, local tenderness and double vision. Complaints of an intense pressure feeling or swelling of the eye associated with nose blowing may also be reported.

Critical signs of recent blow-out fracture include:

edema and ecchymosis of the lid tissues
restriction of ocular motility, especially with vertical movements
orbital crepitus (subcutaneous emphysema)
hypoesthesia of the ipsilateral cheek, due to entrapment of the infraorbital nerve.

There may also be an associated nosebleed due to communication between the orbit and maxillary sinus. Orbital edema initially surrounds and displaces the globe, in some cases causing the eye to appear proptotic. However, as the swelling subsides, the eye is likely to drop down and back, becoming enophthalmic. Associated traumatic uveitis and/or hyphema may be noted as well.

In some cases, patients suffering orbital blow-out fracture initially ignore treatment, and may present long after the initial inflammatory manifestations of trauma have subsided. In these patients, evaluation reveals only relative enophthalmos and motility restriction, usually in upgaze, and possible infraorbital hypoesthesia.

PATHOPHYSIOLOGY
Blow-out fracture may result in cases of abrupt trauma to the eye by any object >5cm in diameter. Because the orbital rim is very strong, the forces of blunt trauma are reflected back, compressing the eye and creating a tremendous increase in pressure within the orbit.

Since the larger bones which comprise the orbit contain sinuses, the orbital walls are at great risk for fracture; should the trauma be of sufficient force, these walls can literally "blow out." The medial wall (ethmoid bone) is occasionally affected. But most commonly, the orbital floor (the superior aspect of the maxillary bone) sustains the damage. In cases of floor fractures, the eye may partially drop down into the maxillary sinus, causing enophthalmos and entrapment of the inferior rectus or inferior oblique muscle.

This entrapment leads to a tethering effect, resulting in a limited downgaze ability and, more notably, an inability toward upgaze in the affected eye. While this situation can be surgically corrected in the early stages, prolonged entrapment leads to fibrosis of the muscle(s) and permanent motility impairment. Associated medial wall fractures may induce damage to the medial rectus muscle and/or the lacrimal apparatus, but this is uncommon.

In most cases, these fractures result in orbital emphysema, creating a direct communication between the ethmoid sinus and the orbit. This produces the feeling of pressure within the orbit when the patient attempts to blow his/her nose. The greatest risk to consider with medial wall fractures is orbital cellulitis, secondary to sinus infection, should pathogenic organisms within the sinus invade the post-tarsal eyelid.

MANAGEMENT
All cases of blunt ocular trauma with resultant crepitus or motility restriction warrant orbital imaging studies. Computed tomography (CT scan) is the procedure of choice. CT is better at imaging the bony structures of the orbit than either plain skull films (X-ray) or MRI. Obtain both axial and coronal scans.

Should you discover a floor fracture with associated herniation of the orbital contents, consider surgical intervention. Generally, surgery is only for patients with recent trauma who manifest significant diplopia in primary gaze or downgaze, or in cases of cosmetically unacceptable enophthalmos. Most oculoplastic specialists will wait 10 to 14 days following the trauma to allow for resolution of the associated edema and hemorrhage. The treatment consists of surgical resection of the periosteum and repair of the fracture, utilizing a bone graft or synthetic material such as silicon or Teflon.

Long-standing entrapment of the extraocular muscles leads to fibrosis and irreversible scarring; intervention to improve motility after four weeks is typically unsuccessful. Initiate prophylactic antibiotic therapy immediately in the event of associated medial wall fractures with orbital emphysema, or if there is any suspicion of ethmoid damage. A broad spectrum oral preparation such as cephalexin or erythromycin (250-500mg QID) may be used for 10 to 14 days. Surgical repair of the medial wall is unnecessary in uncomplicated ethmoid fractures, since the condition resolves spontaneously in three to four weeks.

CLINICAL PEARLS

Cases of orbital blow-out fracture do not constitute an emergency, however, accurate diagnosis and management of the associated ocular manifestations is paramount.
One test that is very helpful in differentiating muscle entrapment in orbital fracture from other muscle or nerve complications is the forced duction test. Entrapped muscles will resist forced movements with a forceps or even a cotton-tipped applicator. Again, this test should ideally be performed after resolution of the orbital swelling.
Check for crepitus by palpating the bony rim of the orbit or lid-small bubbles of air will "pop" when compressed.
For long-standing fractures in which the patient experiences diplopia in downgaze, but is not a surgical candidate, consider incorporating unilateral pr

Pediculosis & Phthiriasis  

SIGNS AND SYMPTOMS
Pediculosis is an eyelid infestation by either Pediculus humanus corporis (body) or Pediculus humanus capitus (head). Phthiriasis, which is actually the most common eyelid infestation, is caused by Phthirus pubis (pubic lice, sometimes referred to as crab lice).

Pediculus are 2 to 4 mm long, and typically infest the hair of the patient. Infestation of the cilia is rare and only occurs in the worst cases. Phthirus are 2mm long, and have a broad-shaped, crab-like body. Its thick, clawed legs make it less mobile than the Pediculus species and lend it to infesting areas where the adjacent hairs are within its grasp (eyelashes, beard, chest, axillary region, pubic region). They rarely infest the scalp.

Ocular signs and symptoms include visible organisms on the scalp, hair, eyelashes or beard; visible blue skin lesions (louse bites); reddish brown deposits (louse feces); secondary blepharitis with preauricular adenopathy; follicular conjunctivitis; and, in severe cases, marginal keratitis. The patient often complains of bilateral ocular itching and irritation.

PATHOPHYSIOLOGY
The Pediculus and Phthirus organisms look similar the each other and interbreed freely. Both types lay eggs on the hair shafts and remain firmly adherent, resisting both mechanical and chemical removal. The Pediculus organism moves well and can be passed from person to person by either close contact or by contact with contaminated bedding. Conversely, Phthiriasis are slow moving, and cannot typically be passed unless cilia is brought into close proximity with infested cilia. Both species are associated with crowded conditions or poor personal hygiene.

MANAGEMENT
Begin management by removing all visible organisms and nits (eggs) with forceps. Place the removed debris in an alcohol wipe and discard it promptly. Instruct the patient to use a pediculocidic-medicated shampoo such as Rid (a safe, effective, non-prescription pediculoside), Lidane 1% (gamma benzene hexachloride), Permethrin 1%, A-200 Pyrinate (pyrethrins, piperonyl butoxide, kerosene), Kwell or Nix.

Topical ocular therapy may include any of the following:

smothering the lice and nits with petroleum jelly or other bland ointments, TID
mercuric oxide 1% or ammoniated mercuric oxide 3%, BID
cholinesterase inhibitors such as physostigmine

Typically, the nits will survive a single application of these agents.

CLINICAL PEARLS

Daily follow up is required for seven to ten days, as nits hatch every seven to ten days.
Instruct patients to thoroughly wash all clothing and linens that may have been exposed to the organism, and educate patients about the transmission of the disease, advising them to refrain from interpersonal contact until the disease is 100 percent resolved. Also counsel patients to educate their recent sexual partners about possible exposure.
Due to ocular toxicity, pediculocide shampoos cannot be used to remove organisms from the eyelid.

Herpes Zoster Ophthalmicus

SIGNS AND SYMPTOMS
Herpes zoster ophthalmicus (HZO) typically presents with nondescript facial pain, fever and general malaise. About four days after onset, a vesicular skin rash appears along the distribution of the fifth cranial nerve, characteristically respecting the vertical midline. The vesicles will discharge fluid and begin to scab over after about one week. The pain is extreme during the inflammatory stage, and patients are tremendously symptomatic.

Ocular involvement may include follicular conjunctivitis, epithelial and/or interstitial keratitis, dendritic keratitis, uveitis, scleritis or episcleritis, chorioretinitis, optic neuropathy, and even neurogenic motility disorders (especially fourth cranial nerve palsy). If you see vesicles at the tip of the nose (known as Hutchinson’s Sign), there is a 75 percent likelihood of ocular sequelae.

PATHOPHYSIOLOGY
HZO occurs when the trigeminal ganglion is invaded by the herpes zoster virus, a varicella-type virus which is usually referred to as “chicken pox” in children or “shingles” in adults. The virus remains dormant in trigeminal nerve cells, and can become reactivated years later by a reduction in the immune system.

Neuronal spread of the virus occurs along the ophthalmic (1st) and less frequently the maxillary (2nd) division of the fifth cranial nerve. Vesicular eruptions occur at the terminal points of sensory innervation, causing extreme pain. Nasociliary involvement will most likely cause ocular inflammation, typically affecting the tissues of the anterior segment. Contiguous spread of the virus may lead to the involvement of other cranial nerves, resulting in optic neuropathy (cranial nerve II) or isolated cranial nerve palsies (cranial nerve III, IV or VI).

MANAGEMENT
The systemic component of this disorder is best treated with oral acyclovir, (Zovirax), 600 to 800mg five times a day for seven to 10 days, starting as soon as the condition is diagnosed. Recently, famciclovir (Famvir) 500mg p.o. t.i.d. has been shown to be as effective in treating herpes zoster ophthalmicus as acyclovir 800mg fives times per day. Timing is crucial, however, to avoid post-herpetic neuralgia. To achieve maximal benefit from oral anti-viral medications, you must start therapy within 72 hours of vesicular eruption. Otherwise, the patient is at risk for developing post-herpetic neuralgia and the beneficial effects of oral anti-viral therapy are lost. You may also wish to prescribe oral steroids to alleviate pain and associated facial edema. If so, try 40 to 60mg of prednisone daily, tapered slowly over 10 days. To treat the skin lesions, applying an antibiotic-steroid ointment, such as Pred-G, to the affected areas twice daily, may help.

Ocular management depends on the severity and tissues involved. In most cases which involve uveitis or keratitis, use cycloplegia (homatropine 5% t.id./q.i.d. or scopolamine 0.25%) b.i.d./q.i.d. After ruling out herpes simplex, it’s also possible to prescribe a topical steroid such as Vexol or Pred Forte q2-q.h. In any compromised eye, prophylaxis with a broad-spectrum antibiotic is a good idea. Finally, palliative treatment consisting simply of cool compresses, and oral analgesics in extreme cases, can be comforting. Cimetidine 400mg p.o. b.i.d may provide some additional relief from the neuralgia; why this works is not entirely understood.

CLINICAL PEARLS

People over age 70 have a much greater chance of HZO infection. Also, those who are immunocompromised due to lymphoma, AIDS, Lyme disease, etc. are at an increased risk.
Ocular involvement varies greatly and is often confusing in the early stages.
Take extreme care when differentiating this condition from herpes simplex virus (HSV), particularly when there is corneal involvement. One key consideration is that the dendritic keratitis which occurs in HZO is infiltrative, while the HSV dendrites are ulcerative.
Also keep in mind the possibility of more involved and complex ocular sequelae (chorioretinitis, optic neuropathy, cranial nerve palsies, uveitic glaucoma), and apply appropriate management strategies in these cases.
Start oral anti-viral therapy within 72 hours of vesicular eruption to possibly avoid post-herpetic neuralgia.

Chalazion

  SIGNS AND SYMPTOMS
Patients will present with one or many focal, hard, painless nodules in the upper or lower eyelid. They may report some enlargement over time, and there may be a history of a painful lid infection prior to the chalazion development, but this isn't always the case. Chalazia are often recurrent, especially in cases of poor lid hygiene or concurrent blepharitis.

PATHOPHYSIOLOGY
A chalazion is a non-infectious, granulomatous inflammation of the meibomian glands. The nodule itself consists of many types of steroid-responsive immune cells, including connective tissue macrophages known as histiocytes, multinucleate giant cells, plasma cells, polymorphonuclear leukocytes and eosinophils.

A chalazion may be a residual aggregation of inflammatory cells following an eyelid infection such as hordeola and preseptal cellulitis, or may develop from the retention of meibomian gland secretions.

MANAGEMENT
Chalazia are non-infectious collections of immune cells that require intensive steroid therapy. Because chalazia reside deep under the skin, no topical medications will be able to penetrate sufficiently. About 25 percent of chalazia resolve spontaneously. For those that don't, instruct the patient to apply a hot compress to open the glands, then to digitally massage the area to break and express the nodule, up to four times a day.

If this is ineffective, inject triamcinolone acetonide (Kenalog) 5mg/ml or 10mg/ml directly into the chalazion (some practitioners have advocated concentrations as high as 40mg/ml, but this is not standard practice). Approach the lesion from the palpebral side, and inject 0.05 to 0.3ml in standard form, using a tuberculin syringe and 30-gauge needle. You may want to use a chalazion clamp and topical anesthesia, but this is not absolutely necessary. Usually the patient is markedly better one week later, but you may need to re-treat extremely large chalazia. If the chalazia persists even after a second steroid injection, or if the patient cannot tolerate the procedure, excise the remaining lesion using a curette under local anesthesia as a last resort.

CLINICAL PEARLS

Intralesional steroid injection is contraindicated for patients with dark skin, since the procedure can cause depigmentation which often persists for months, or is permanent. This is especially likely if the point of injection is on the skin, but may occur even if injecting through the palpebral conjunctiva.
Biopsy any recurrent chalazia, especially those following surgical excision, to rule out a particularly deadly malignancy known as sebaceous gland carcinoma.
  SIGNS AND SYMPTOMS
Patients will present with one or many focal, hard, painless nodules in the upper or lower eyelid. They may report some enlargement over time, and there may be a history of a painful lid infection prior to the chalazion development, but this isn't always the case. Chalazia are often recurrent, especially in cases of poor lid hygiene or concurrent blepharitis.

PATHOPHYSIOLOGY
A chalazion is a non-infectious, granulomatous inflammation of the meibomian glands. The nodule itself consists of many types of steroid-responsive immune cells, including connective tissue macrophages known as histiocytes, multinucleate giant cells, plasma cells, polymorphonuclear leukocytes and eosinophils.

A chalazion may be a residual aggregation of inflammatory cells following an eyelid infection such as hordeola and preseptal cellulitis, or may develop from the retention of meibomian gland secretions.

MANAGEMENT
Chalazia are non-infectious collections of immune cells that require intensive steroid therapy. Because chalazia reside deep under the skin, no topical medications will be able to penetrate sufficiently. About 25 percent of chalazia resolve spontaneously. For those that don't, instruct the patient to apply a hot compress to open the glands, then to digitally massage the area to break and express the nodule, up to four times a day.

If this is ineffective, inject triamcinolone acetonide (Kenalog) 5mg/ml or 10mg/ml directly into the chalazion (some practitioners have advocated concentrations as high as 40mg/ml, but this is not standard practice). Approach the lesion from the palpebral side, and inject 0.05 to 0.3ml in standard form, using a tuberculin syringe and 30-gauge needle. You may want to use a chalazion clamp and topical anesthesia, but this is not absolutely necessary. Usually the patient is markedly better one week later, but you may need to re-treat extremely large chalazia. If the chalazia persists even after a second steroid injection, or if the patient cannot tolerate the procedure, excise the remaining lesion using a curette under local anesthesia as a last resort.

CLINICAL PEARLS

Intralesional steroid injection is contraindicated for patients with dark skin, since the procedure can cause depigmentation which often persists for months, or is permanent. This is especially likely if the point of injection is on the skin, but may occur even if injecting through the palpebral conjunctiva.
Biopsy any recurrent chalazia, especially those following surgical excision, to rule out a particularly deadly malignancy known as sebaceous gland carcinoma.

Preseptal Cellulitis

  SIGNS AND SYMPTOMS
Patients with preseptal cellulitis will present with an acutely painful, swollen eyelid. Because of the pronounced edema, the patient may not be able to open his or her eyes. However, there will be no disturbance in visual acuity or ocular motility, nor any signs of proptosis. There may be a concurrent history of sinus infection or congestion, penetrating trauma to the eyelid, or dental infection. In most cases, the patient will be systemically well and afebrile (not feverish).

PATHOPHYSIOLOGY
The eyelid is separated into preseptal and postseptal areas by the orbital septum, which prevents the spread of infection to the orbit and central nervous system. Preseptal cellulitis is a bacterial infection of the eyelid anterior to the orbital septum. The routes of infection include direct inoculation from trauma, or spread of infection from the neighboring ethmoid sinus or teeth.

The most commonly encountered organisms include Staphylococcus aureus, Streptococcus pyogenes and Streptococcus pneumoniae. If a human or animal bite wound is the source, suspect anaerobic bacteria such as Peptostreptococcus and Bacteroides. If the infection spreads posterior to the orbital septum, it may result in a postseptal (or orbital) cellulitis, with associated vision loss, ocular motility restrictions and proptosis. Patients with orbital cellulitis are systemically ill and febrile.

MANAGEMENT
To prevent the possibly disastrous spread of infection to the postseptal area, it is crucial to quickly suppress the infection. Oral therapy is necessary; topical antibiotics alone are insufficient. Amoxicillin 500mg PO TID is an excellent choice, although you may substitute nafacillin, oxacillin or cefazolin. If the cause is a bite wound, consider ampicillin or clindamycin. In cases of concurrent sinus infection, you may wish to consult an otolaryngologist to help you identify the involved organism.

CLINICAL PEARLS

Often, insect bites can mimic preseptal cellulitis, but these are rarely infectious. Instead, the patient will have a severe local allergic reaction. If the lid is not extremely painful upon palpation, it is usually an insect bite. A short course of oral antihistamines or steroids and cold compresses will often be sufficient. If you are in doubt as to the infectious nature of an insect bite, proceed with oral antibiotic therapy as well.

Lacrimal gland inflammation (dacryoadenitis) can also mimic preseptal cellulitis. Though rare, it usually occurs in adolescent viral infections such as mumps, influenza and measles.

Hordeolum

  SIGNS AND SYMPTOMS
Patients will present with an acutely swollen and edematous upper or lower eyelid. Visual function will be normal. There may be an associated conjunctivitis and possibly mucopurulent discharge. The lids will be extremely sensitive to palpation, and there may be an associated pustular, pimple-like lesion at the lid margin or, less commonly, at the dermis.

PATHOPHYSIOLOGY
A hordeolum is a bacterial infection of either the meibomian glands or ciliary glands (the glands of Zeis and Moll). If the latter are involved, the hordeolum is considered external and appears focal in nature. If the deeper meibomian glands are involved, the hordeolum is considered internal and is less circumscribed in appearance. Staphylococcus aureus and Staphylococcus epidermidis are the most likely culprits. Acute and chronic inflammation associated with hordeola, especially if improperly treated, may result in a granulomatous inflammation known as chalazia. If the infection spreads to neighboring glands or other lid tissue anterior to the tarsal plate, it may lead to preseptal cellulitis.

MANAGEMENT
Traditionally, the standard treatment has been topical antibiotic solutions and ointments. Unfortunately, this has virtually no therapeutic benefit. Topical application does not supply enough intra-tissue concentrations of antibiotics to be effective. Oral antibiotic therapy is necessary. If the hordeolum is external, you may drain and lance the lesion (anesthetic is usually unnecessary) or epilate nearby lashes to enhance drainage. Digital expression of purulent material in your office will expedite healing, but is not absolutely necessary. Antibiotic therapy could include dicloxacillin 250mg PO Q6H, erythromycin or tetracycline 250mg PO QID or amoxacillin 500mg PO TID for 10 days. Cold compresses will help to suppress inflammation.

CLINICAL PEARLS

The most common misdiagnosis of hordeola is chalazia. The distinguishing factor is pain upon palpation. If the lesion is not intensely sensitive to palpation, most likely it's a chalazion.
Avoid traditional topical therapies, which are therapeutically ineffective, and begin immediately with oral medications.

Hordeolum

  SIGNS AND SYMPTOMS
Patients will present with an acutely swollen and edematous upper or lower eyelid. Visual function will be normal. There may be an associated conjunctivitis and possibly mucopurulent discharge. The lids will be extremely sensitive to palpation, and there may be an associated pustular, pimple-like lesion at the lid margin or, less commonly, at the dermis.

PATHOPHYSIOLOGY
A hordeolum is a bacterial infection of either the meibomian glands or ciliary glands (the glands of Zeis and Moll). If the latter are involved, the hordeolum is considered external and appears focal in nature. If the deeper meibomian glands are involved, the hordeolum is considered internal and is less circumscribed in appearance. Staphylococcus aureus and Staphylococcus epidermidis are the most likely culprits. Acute and chronic inflammation associated with hordeola, especially if improperly treated, may result in a granulomatous inflammation known as chalazia. If the infection spreads to neighboring glands or other lid tissue anterior to the tarsal plate, it may lead to preseptal cellulitis.

MANAGEMENT
Traditionally, the standard treatment has been topical antibiotic solutions and ointments. Unfortunately, this has virtually no therapeutic benefit. Topical application does not supply enough intra-tissue concentrations of antibiotics to be effective. Oral antibiotic therapy is necessary. If the hordeolum is external, you may drain and lance the lesion (anesthetic is usually unnecessary) or epilate nearby lashes to enhance drainage. Digital expression of purulent material in your office will expedite healing, but is not absolutely necessary. Antibiotic therapy could include dicloxacillin 250mg PO Q6H, erythromycin or tetracycline 250mg PO QID or amoxacillin 500mg PO TID for 10 days. Cold compresses will help to suppress inflammation.

CLINICAL PEARLS

The most common misdiagnosis of hordeola is chalazia. The distinguishing factor is pain upon palpation. If the lesion is not intensely sensitive to palpation, most likely it's a chalazion.
Avoid traditional topical therapies, which are therapeutically ineffective, and begin immediately with oral medications.

Examination of the Extremities and Back

Equipment Needed

None

General Considerations

The patient should be undressed and gowned as needed for this examination.
Some portions of the examination may not be appropriate depending on the clinical situation (performing range of motion on a fractured leg for example).
The musculoskeletal exam is all about anatomy. Think of the underlying anatomy as you obtain the history and examine the patient.
When taking a history for an acute problem always inquire about the mechanism of injury, loss of function, onset of swelling (< 24 hours), and initial treatment.
When taking a history for a chronic problem always inquire about past injuries, past treatments, effect on function, and current symptoms.
The cardinal signs of musculoskeletal disease are pain, redness (erythema), swelling, increased warmth, deformity, and loss of function.
Always begin with inspection, palpation and range of motion, regardless of the region you are examining. Specialized tests are often omitted unless a specific abnormality is suspected. A complete evaluation will include a focused neurologic exam of the effected area.

Regional Considerations

Remember that the clavicle is part of the shoulder. Be sure to include it in your examination. [p468]
The patella is much easier to examine if the leg is extended and relaxed. [p473]
Be sure to palpate over the spinous process of each vertebrae. [p477]
It is always helpful to observe the patient standing and walking.
Always consider referred pain, from the neck or chest to the shoulder, from the back or pelvis to the hip, and from the hip to the knee.
Pain with, or limitation of, rotation is often the first sign of hip disease.
Diagnostic hints based on location of pain:


 

Back

Side

Front

Shoulder Pain

Muscle Spasm

Bursitis or Rotator Cuff

Glenohumeral Joint

Hip Pain

Sciatica

Bursitis

Hip Joint


Inspection

Look for scars, rashes, or other lesions. [p464] [1]
Look for asymmetry, deformity, or atrophy.
Always compare with the other side.

Palpation

Examine each major joint and muscle group in turn.
Identify any areas of tenderness. [2]
Identify any areas of deformity.
Always compare with the other side.

Range of Motion

Start by asking the patient to move through an active range of motion (joints moved by patient). Proceed to passive range of motion (joints moved by examiner) if active range of motion is abnormal.

Active

Ask the patient to move each joint through a full range of motion.
Note the degree and type (pain, weakness, etc.) of any limitations.
Note any increased range of motion or instability.
Always compare with the other side.
Proceed to passive range of motion if abnormalities are found.

Passive

Ask the patient to relax and allow you to support the extremity to be examined. ++ [3]
Gently move each joint through its full range of motion.
Note the degree and type (pain or mechanical) of any limitation. [4]
If increased range of motion is detected, perform special tests for instability as appropriate.
Always compare with the other side.

Specific Joints

Fingers - flexion/extension; abduction/adduction [p466]
Thumb - flexion/extension; abduction/adduction; opposition
Wrist - flexion/extension; radial/ulnar deviation [p467]
Forearm - pronation/supination (function of BOTH elbow and wrist) [p468]
Elbow - flexion/extension
Shoulder - flexion/extension; internal/external rotation; abduction/adduction (2/3 glenohumeral joint, 1/3 scapulo-thoracic) [p468] [5]
Hip - flexion/extension; abduction/adduction; internal/external rotation [p474]
Knee - flexion/extension [p473]
Ankle - flexion (plantarflexion)/extension (dorsiflexion) [p470]
Foot - inversion/eversion [p469]
Toes - flexion/extension
Spine - flexion/extension; right/left bending; right/left rotation [p466, p477]

Vascular

Pulses

Check the radial pulses on both sides. If the radial pulse is absent or weak, check the brachial pulses. [p433]
Check the posterior tibial and dorsalis pedis pulses on both sides. If these pulses are absent or weak, check the popliteal and femoral pulses. [p435]

Capillary Refill

Press down firmly on the patient's finger or toe nail so it blanches. ++
Release the pressure and observe how long it takes the nail bed to "pink" up.
Capillary refill times greater than 2 to 3 seconds suggest peripheral vascular disease, arterial blockage, heart failure, or shock.

Vital Signs

Equipment Needed

A Stethoscope
A Blood Pressure Cuff
A Watch Displaying Seconds
A Thermometer

General Considerations

The patient should not have had alcohol, tobacco, caffeine, or performed vigorous exercise within 30 minutes of the exam.
Ideally the patient should be sitting with feet on the floor and their back supported. The examination room should be quiet and the patient comfortable.
History of hypertension, slow or rapid pulse, and current medications should always be obtained.

Temperature

Temperature can be measured is several different ways:

Oral with a glass, paper, or electronic thermometer (normal 98.6F/37C) [p129] [1]
Axillary with a glass or electronic thermometer (normal 97.6F/36.3C)
Rectal or "core" with a glass or electronic thermometer (normal 99.6F/37.7C)
Aural (the ear) with an electronic thermometer (normal 99.6F/37.7C)

Of these, axillary is the least and rectal is the most accurate.

Respiration

Best done immediately after taking the patient's pulse. Do not announce that you are measuring respirations. [p129, p237] [2]
Without letting go of the patients wrist begin to observe the patient's breathing. Is it normal or labored? [p252]
Count breaths for 15 seconds and multiply this number by 4 to yield the breaths per minute.
In adults, normal resting respiratory rate is between 14-20 breaths/minute. Rapid respiration is called tachypnea.

Pulse

Sit or stand facing your patient. [p274]
Grasp the patient's wrist with your free (non-watch bearing) hand (patient's right with your right or patient's left with your left). There is no reason for the patient's arm to be in an awkward position, just imagine you're shaking hands.
Compress the radial artery with your index and middle fingers.
Note whether the pulse is regular or irregular:
Regular - evenly spaced beats, may vary slightly with respiration [p300]
Regularly Irregular - regular pattern overall with "skipped" beats
Irregularly Irregular - chaotic, no real pattern, very difficult to measure rate accurately
Count the pulse for 15 seconds and multiply by 4.
Count for a full minute if the pulse is irregular. [3]
Record the rate and rhythm.

Interpretation

A normal adult heart rate is between 60 and 100 beats per minute (see below for children).
A pulse greater than 100 beats/minute is defined to be tachycardia. Pulse less than 60 beats/minute is defined to be bradycardia. Tachycardia and bradycardia are not necessarily abnormal. Athletes tend to be bradycardic at rest (superior conditioning). Tachycardia is a normal response to stress or exercise.

Blood Pressure

Position the patient's arm so the anticubital fold is level with the heart. Support the patient's arm with your arm or a bedside table. [p277]
Center the bladder of the cuff over the brachial artery approximately 2 cm above the anticubital fold. Proper cuff size is essential to obtain an accurate reading. Be sure the index line falls between the size marks when you apply the cuff. Position the patient's arm so it is slightly flexed at the elbow. [4]
Palpate the radial pulse and inflate the cuff until the pulse disappears. This is a rough estimate of the systolic pressure. [5]
Place the stetescope over the brachial artery. [6]
Inflate the cuff to 30 mmHg above the estimated systolic pressure.
Release the pressure slowly, no greater than 5 mmHg per second.
The level at which you consistantly hear beats is the systolic pressure. [7]
Continue to lower the pressure until the sounds muffle and disappear. This is the diastolic pressure. [8]
Record the blood pressure as systolic over diastolic ("120/70" for example).

Interpretation

Higher blood pressures are normal during exertion or other stress. Systolic blood pressures below 80 may be a sign of serious illness or shock.
Blood pressure should be taken in both arms on the first encounter. If there is more than 10 mmHg difference between the two arms, use the arm with the higher reading for subsequent measurements.
It is frequently helpful to retake the blood pressure near the end of the visit. Earlier pressures may be higher due to the "white coat" effect.
Always recheck "unexpected" blood pressures yourself.


Blood Pressure Classification in Adults

Category

Systolic

Diastolic

Normal

<140 <90 Isolated Systolic Hypertension >140

<90 Mild Hypertension 140-159 90-99 Moderate Hypertension 160-179 100-109 Severe Hypertension 180-209 110-119 Crisis Hypertension >210

>120


In children, pulse and blood pressure vary with the age. The following table should serve as a rough guide:


Average Pulse and Blood Pressure in Normal Children

Age

Birth

6mo

1yr

2yr

6yr

8yr

10yr

Pulse

140

130

115

110

103

100

95

Systolic BP

70

90

90

92

95

100

105




Notes

Page numbers refer to Barbara Bates' A Guide to Physical Examination and History Taking, Sixth Edition , published by Lippincott in 1995.
Unlike pulse, respirations are very much under voluntary control. If you tell the patient you are counting their breaths, they may change their breathing pattern. You cannot tell someone to "breath normally," normal breathing is involuntary.
With an irregular pulse, the beats counted in any 15 second period may not represent the overall rate. The longer you measure, the more these variations are averaged out.
Do not rely on pressures obta