SIGNS AND SYMPTOMS
This nodular inflammation of the peri-limbal tissues occurs secondary to an allergic hypersensitivity response of the cornea. The disease is most common (60 percent of cases) in women during their first and second decades who live in crowded or impoverished quarters.
Patients typically present with symptoms of tearing, ocular irritation, mild to severe photophobia and a history of similar episodes. If the underlying cause is Staphylococcal infection, expect to see a rope-like, mucopurulent discharge as well.
There are two distinct types of phlyctenular lesions: corneal and conjunctival. Under the slit lamp a conjunctival (vascularized) phlyctenule appears as a 1 to 3mm hard, triangular, slightly elevated, yellowish-white nodule surrounded by a hyperemic response, in the vicinity of the inferior limbus. These lesions tend to be bilateral.
Corneal phlyctenules produce more severe symptoms. They usually begin adjacent to the limbus as a white mound, with a radial pattern of vascularized conjunctival vessels. The lesion may then migrate toward the center of the cornea, progressing as a gray-white, superficial ulcer surrounded by infiltrate in the areas where the lesion has been.
PATHOPHYSIOLOGY
The exact mechanism or mechanisms that produce phlyctenules is unclear. Histologically, they are composed of lymphocytes, histocytes and plasma cells. Polymorphonuclear leukocytes are found in necrotic lesions. Their formation seems to be the result of a delayed hypersensitivity reaction to tuberculin protein, Staphylococcus aureus, Coccidioides immitis (a soil-based fungus common in the southwestern U.S.), Chlamydia, acne rosacea, some varieties of interstitial parasites and the fungus Candida albicans. Rarely are cases idiopathic. Such a diagnosis could only be made by exclusion.
MANAGEMENT
Ocular management begins with patient education to improve eyelid hygiene. Lid scrubs two to three times per day along with artificial tears and ointments may soothe and reverse mild cases. Moderate to severe cases require topical steroids or steroid-antibiotic combinations. Cycloplegia is only necessary if there is an associated iritis. In most cases, prednisolone acetate (Pred Forte), one drop, Q2H/QID is sufficient, provided there are no corneal contraindications.
If the suspected etiology is Staph. reaction or acne rosacea, prescribe 250mg of oral tetracycline QID or 250mg erythromycin QID PO, along with topical antibiotic ointments such as bacitracin or erythromycin at bedtime. Topical metronidazole (Metrogel) applied to the skin TID is also effective. Because tetracycline can damage and discolor the teeth of children, it is contraindicated in patients under age 10. In these cases, substitute doxycycline 100mg TID or erythromycin 250mg QID PO. Continue treatment for two to four weeks. In suspicious cases, order a chest X-ray and PPD to rule out tuberculosis.
CLINICAL PEARLS
Maintain the treatment as long as signs and symptoms persist, with follow-up visits weekly. Taper steroids once you see improvement but maintain the antibiotic until the steroid therapy is completely finished. Have patients continue the eyelid hygiene indefinitely.
Other potential differential diagnoses include infiltrates secondary to chronic blepharitis, inflamed pingueculum, herpes simplex and infectious or sterile corneal ulcer. The resurgence of tuberculosis infection makes TB testing almost mandatory.
Wednesday, December 29, 2010
Saturday, December 25, 2010
Sterile Corneal Infiltrates
SIGNS AND SYMPTOMS
Unlike bacterial corneal ulcer patients, marginal sterile corneal ulcer patients present with only mild conjunctival injection, little to no conjunctival chemosis, ocular irritation and normal vision. One or more marginal subepithelial corneal infiltrates are common in many conditions, and usually do not warrant much concern. Accompanying sequelae may include mild iritis, folds in Descemet's membrane if there is substantial corneal edema, and posterior synechiae in chronic cases.
Patients with Staphylococcal hypersensitivity reactions may present without symptoms. Here, scattered multiple areas of sub-epithelial and anterior stromal infiltrates, with or without epithelial defects, line the limbal area (mostly inferiorly). The entity is usually bilateral. One distinct characteristic is the notable clear zone that lies between the areas of infiltrate and the limbus.
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. Other known associations are vernal keratitis, vitamin A-deficiency and contact lens solution reaction. The principle differential diagnoses include infectious corneal ulcer, marginal sub-epithelial infiltrates secondary to contact lens wear and Mooren's marginal corneal ulcer.
PATHOPHYSIOLOGY
Sterile infiltrates usually represent a low-grade immune response to bacterial exotoxins. For bacterial infection or inflammation to occur, the microorganism must be able to adhere to the corneal surface. Staphylococcus aureus, Streptococcus pneumoniae and Pseudomonas aeruginosa are significantly more adherent than other organisms, possibly accounting for their more frequent involvement in corneal disease.. These organisms are more adherent to the cornea and are tightly adherent to themselves, providing a resistance to phagocytosis by host inflammatory cells.
Staph. aureus is recognized as one of the common opportunistic ocular pathogens. The organism is a gram-positive non-encapsulated coccus capable of producing a variety of exotoxins and enzymes. In addition to its ability to infect the central cornea, it is a leading cause of sterile marginal keratitis.
Powerful exotoxins released by bacteria colonizing the eyelid margin induce peripheral corneal destruction through antigen-antibody reactions. Polymorphonuclear leukocytes and fibroblasts, which migrate to the area to help fight exotoxins, produce collagenase and proteoglycanase enzymes that often produce additional damage.
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. Eyelid scrubs BID/TID using commercially available lid scrubs or baby shampoo will begin the process of cleansing the lid margins.
To fully eradicate dense colonies of lid margin bacteria, prescribe a topical aminoglycoside (gentamicin, tobramycin) or fluoroquinolone (ciprofloxacin, norfloxacin, ofloxacin) QID. The antibiotics kill the bacteria and also mechanically wash organisms and their toxins away from the eyelid margin. If the patient complains of discomfort, prescribe a cycloplegic. Rx a topical steroid based on the severity of the condition.
CLINICAL PEARLS
Since the corneal tissue is free from infection and its damage originates from the secondary effects of inflammation, the most expeditious treatment is both topical antibiotics and topical anti-inflammatories. Many practitioners are apprehensive about prescribing topical steroids in the face of corneal epithelial compromise, although this does not usually pose a serious threat. Nevertheless, if you prefer a more conservative approach, begin with antibiotic treatment alone for 24 to 48 hours, then judiciously add a topical steroid thereafter and monitor for IOP rise.
Today, there is debate regarding the need to culture before starting treatment. Because culture results are not available for 24 to 48 hours, many believe it is only necessary when a condition fails to respond to the prescribed therapy. We advocate treating immediately and then culturing if the condition does not improve or worsens within the first 48 to 72 hours.
Unlike bacterial corneal ulcer patients, marginal sterile corneal ulcer patients present with only mild conjunctival injection, little to no conjunctival chemosis, ocular irritation and normal vision. One or more marginal subepithelial corneal infiltrates are common in many conditions, and usually do not warrant much concern. Accompanying sequelae may include mild iritis, folds in Descemet's membrane if there is substantial corneal edema, and posterior synechiae in chronic cases.
Patients with Staphylococcal hypersensitivity reactions may present without symptoms. Here, scattered multiple areas of sub-epithelial and anterior stromal infiltrates, with or without epithelial defects, line the limbal area (mostly inferiorly). The entity is usually bilateral. One distinct characteristic is the notable clear zone that lies between the areas of infiltrate and the limbus.
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. Other known associations are vernal keratitis, vitamin A-deficiency and contact lens solution reaction. The principle differential diagnoses include infectious corneal ulcer, marginal sub-epithelial infiltrates secondary to contact lens wear and Mooren's marginal corneal ulcer.
PATHOPHYSIOLOGY
Sterile infiltrates usually represent a low-grade immune response to bacterial exotoxins. For bacterial infection or inflammation to occur, the microorganism must be able to adhere to the corneal surface. Staphylococcus aureus, Streptococcus pneumoniae and Pseudomonas aeruginosa are significantly more adherent than other organisms, possibly accounting for their more frequent involvement in corneal disease.. These organisms are more adherent to the cornea and are tightly adherent to themselves, providing a resistance to phagocytosis by host inflammatory cells.
Staph. aureus is recognized as one of the common opportunistic ocular pathogens. The organism is a gram-positive non-encapsulated coccus capable of producing a variety of exotoxins and enzymes. In addition to its ability to infect the central cornea, it is a leading cause of sterile marginal keratitis.
Powerful exotoxins released by bacteria colonizing the eyelid margin induce peripheral corneal destruction through antigen-antibody reactions. Polymorphonuclear leukocytes and fibroblasts, which migrate to the area to help fight exotoxins, produce collagenase and proteoglycanase enzymes that often produce additional damage.
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. Eyelid scrubs BID/TID using commercially available lid scrubs or baby shampoo will begin the process of cleansing the lid margins.
To fully eradicate dense colonies of lid margin bacteria, prescribe a topical aminoglycoside (gentamicin, tobramycin) or fluoroquinolone (ciprofloxacin, norfloxacin, ofloxacin) QID. The antibiotics kill the bacteria and also mechanically wash organisms and their toxins away from the eyelid margin. If the patient complains of discomfort, prescribe a cycloplegic. Rx a topical steroid based on the severity of the condition.
CLINICAL PEARLS
Since the corneal tissue is free from infection and its damage originates from the secondary effects of inflammation, the most expeditious treatment is both topical antibiotics and topical anti-inflammatories. Many practitioners are apprehensive about prescribing topical steroids in the face of corneal epithelial compromise, although this does not usually pose a serious threat. Nevertheless, if you prefer a more conservative approach, begin with antibiotic treatment alone for 24 to 48 hours, then judiciously add a topical steroid thereafter and monitor for IOP rise.
Today, there is debate regarding the need to culture before starting treatment. Because culture results are not available for 24 to 48 hours, many believe it is only necessary when a condition fails to respond to the prescribed therapy. We advocate treating immediately and then culturing if the condition does not improve or worsens within the first 48 to 72 hours.
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. Photophobia and epiphora are common; however, vision may or may not be affected, depending upon the location and extent of the corneal lesion. You may see a vesicular skin rash and follicular conjunctivitis with the initial infection, but these are less common with recurrent HSV. A more common sign is secondary uveitis.
A dendritic corneal ulcer is the hallmark sign of HSV infection, accompanied by stromal keratitis in more severe presentations. These ulcers may begin as nondescript punctate keratopathies, but quickly coalesce to form the familiar branching patterns which stain brightly with sodium fluorescein dye. Because the virus invades and compromises the epithelial cells surrounding the ulcer, the leading edges (the so-called "terminal end-bulbs") will stain with rose bengal or lissamine green.
Pathophysiology
Herpes simplex is actually the most common virus found in humans. It is transmitted via bodily fluids, usually saliva, and may affect the skin and mucous membranes of the host. Primary infections occur most often in children between the ages of 6 months and 5 years. It typically manifests as a vesicular rash, sometimes affecting the skin of the lids but more commonly resulting in a "fever blister" or "cold sore" in or around the mouth.
After resolution, the virus remains dormant in the body of the host and can be reactivated in as many as 25 percent of cases by fever, trauma, stress, immunosuppressive agents or exposure to ultraviolet radiation. In recurrent attacks, the virus invades and replicates within the corneal epithelium. As the cells die, an ulcerative keratitis results. Disciform stromal scarring, conjunctivitis and uveitis are common sequelae.
Management
Corneal epithelial disease secondary to HSV infection must be managed aggressively and quickly to prevent deeper penetration. The treatment of choice is topical trifluridine 1% given at two hour intervals, nine times daily. As the dendrites begin to regress, taper the dosage to q3-4h until the lesion resolves completely (usually in seven to 10 days). At this point, however, have the patient continue the medication t.i.d. for another week to ensure suppression of the virus.
Some practitioners recommend debriding the ulcer bed to remove active virus cells, but this has not been definitively proven to hasten resolution or improve the final visual outcome. You may also need to prescribe a cycloplegic (homatropine 2% t.i.d.-q.i.d. or scopolamine 0.25% b.i.d.-q.i.d.), again depending upon the severity of the uveitic response. Avoid topical steroids in cases of active epithelial HSV keratitis. Studies show that the virus replicates more rapidly in the presence of steroids, prolonging the course of the disease. The use of oral acyclovir (400mg 5x/day) or another oral antiviral for recalcitrant ulcers has yet to be proven clinically significant. However, it has been shown recently that the use of oral acyclovir 400mg q.d. significantly reduces the recurrence of herpes simplex keratitis in imunocompetent patients. At this point, 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.
A new development in the management of herpes simplex keratitis has come in the form of topical acyclovir ointment (Zovirax). Place the ointment in the lower cul-de-sac five times per day at four hour intervals. At this point, toxicity seems to be low.
Clinical Pearls
Suspect HSV in cases of unilateral adult-onset red eye that is inconsistent with the symptoms (i.e., the patient seems to be in far less discomfort than the appearance of the eye would indicate), particularly if the individual has a previous history of similar "infections."
Each recurrent attack induces greater damage to the corneal nerves, leading to hypoesthesia (reduced corneal sensitivity). The cotton-wisp test for corneal sensitivity is invariably positive in cases of HSV keratitis; use it whenever in doubt. Also, consider a history of prolonged sun exposure or extreme psychological stress to be significant in diagnosing HSV.
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. Photophobia and epiphora are common; however, vision may or may not be affected, depending upon the location and extent of the corneal lesion. You may see a vesicular skin rash and follicular conjunctivitis with the initial infection, but these are less common with recurrent HSV. A more common sign is secondary uveitis.
A dendritic corneal ulcer is the hallmark sign of HSV infection, accompanied by stromal keratitis in more severe presentations. These ulcers may begin as nondescript punctate keratopathies, but quickly coalesce to form the familiar branching patterns which stain brightly with sodium fluorescein dye. Because the virus invades and compromises the epithelial cells surrounding the ulcer, the leading edges (the so-called "terminal end-bulbs") will stain with rose bengal or lissamine green.
Pathophysiology
Herpes simplex is actually the most common virus found in humans. It is transmitted via bodily fluids, usually saliva, and may affect the skin and mucous membranes of the host. Primary infections occur most often in children between the ages of 6 months and 5 years. It typically manifests as a vesicular rash, sometimes affecting the skin of the lids but more commonly resulting in a "fever blister" or "cold sore" in or around the mouth.
After resolution, the virus remains dormant in the body of the host and can be reactivated in as many as 25 percent of cases by fever, trauma, stress, immunosuppressive agents or exposure to ultraviolet radiation. In recurrent attacks, the virus invades and replicates within the corneal epithelium. As the cells die, an ulcerative keratitis results. Disciform stromal scarring, conjunctivitis and uveitis are common sequelae.
Management
Corneal epithelial disease secondary to HSV infection must be managed aggressively and quickly to prevent deeper penetration. The treatment of choice is topical trifluridine 1% given at two hour intervals, nine times daily. As the dendrites begin to regress, taper the dosage to q3-4h until the lesion resolves completely (usually in seven to 10 days). At this point, however, have the patient continue the medication t.i.d. for another week to ensure suppression of the virus.
Some practitioners recommend debriding the ulcer bed to remove active virus cells, but this has not been definitively proven to hasten resolution or improve the final visual outcome. You may also need to prescribe a cycloplegic (homatropine 2% t.i.d.-q.i.d. or scopolamine 0.25% b.i.d.-q.i.d.), again depending upon the severity of the uveitic response. Avoid topical steroids in cases of active epithelial HSV keratitis. Studies show that the virus replicates more rapidly in the presence of steroids, prolonging the course of the disease. The use of oral acyclovir (400mg 5x/day) or another oral antiviral for recalcitrant ulcers has yet to be proven clinically significant. However, it has been shown recently that the use of oral acyclovir 400mg q.d. significantly reduces the recurrence of herpes simplex keratitis in imunocompetent patients. At this point, 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.
A new development in the management of herpes simplex keratitis has come in the form of topical acyclovir ointment (Zovirax). Place the ointment in the lower cul-de-sac five times per day at four hour intervals. At this point, toxicity seems to be low.
Clinical Pearls
Suspect HSV in cases of unilateral adult-onset red eye that is inconsistent with the symptoms (i.e., the patient seems to be in far less discomfort than the appearance of the eye would indicate), particularly if the individual has a previous history of similar "infections."
Each recurrent attack induces greater damage to the corneal nerves, leading to hypoesthesia (reduced corneal sensitivity). The cotton-wisp test for corneal sensitivity is invariably positive in cases of HSV keratitis; use it whenever in doubt. Also, consider a history of prolonged sun exposure or extreme psychological stress to be significant in diagnosing HSV.
Bacterial Keratitis
SIGNS AND SYMPTOMS
The patient will present with a unilateral, acutely painful, photophobic, intensely injected eye. Visual acuity is usually reduced, and profuse tearing is common. There will be a focal stromal infiltrate with an overlying area of epithelial excavation. There is likely to be thick, ropy, mucopurulent discharge.
The cornea will be very edematous. The conjunctival and episcleral vessels will be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal defect. In severe cases, there will be a pronounced anterior chamber reaction, often with hypopyon. Intraocular pressure may be low due to secretory hypotony of the ciliary body, but most often will be elevated due to blockage of the trabecular meshwork by inflammatory cells. Often, the eyelids will also be edematous.
PATHOPHYSIOLOGY
Once the corneal defenses are breached, specifically the epithelial glycocalyx, the cornea is prone to infection. Possible causes include direct corneal trauma, chronic eyelid disease, tear film abnormalities affecting the ocular surface and hypoxic trauma from contact lens wear. Pathogenic bacteria colonize the corneal stroma and immediately become antigenic, both directly and indirectly, by releasing enzymes and toxins.
This sets up an antigen-antibody immune reaction which leads to an inflammatory reaction. The body releases polymorphonuclear leukocytes (PMNs) which aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize and digest the bacteria. The collagen stroma is poorly tolerant of the bacterial and leukocytic enzymes and undergoes degradation, necrosis and thinning. This results in scarring of the cornea. With severe thinning the cornea may perforate, creating the possibility for endophthalmitis.
Throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus aureus. However, in cases involving contact lens wear and cosmetics, the most common infective organism is Pseudomonas aeruginosa.
MANAGEMENT
As with bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting organism but is often difficult or impractical. First and foremost, you must halt bacterial proliferation; do not delay treatment while waiting for the culture results. If you have the materials available, scrape the ulcer using a platinum spatula and plate the specimen onto blood and chocolate agar culture media. A simpler but less effective method is to use a culturette.
Regardless, immediately begin therapy with a broad spectrum antibiotic. A popular initial therapy is the fluoroquinolone ciprofloxacin 0.3% (Ciloxan) two drops every 15 minutes for six hours, followed by two drops every 30 minutes for 18 hours, and then tapered depending on patient response. Another fluoroquinolone, ofloxacin 0.3% (Ocuflox) is also an effective treatment for bacterial keratitis. Both fluoroquinolones are as effective at managing bacterial keratitis as fortified antibiotics, but with significantly fewer side effects.
To increase patient comfort and minimize inflammation, strong cycloplegia is mandatory. Begin with a cycloplegic such as scopolamine 0.25% TID. If this is insufficient, switch to atropine 1% BID. Adjunctive use of cold compresses will also help to reduce inflammation. If there is evidence of secondary inflammatory glaucoma, Rx a topical beta-blocker BID.
Have the patient return daily for follow-up visits. Once the infection is controlled, add a topical steroid Q2H to the regimen. Continue the daily follow-up and begin to taper all medications as you see improvement.
CLINICAL PEARLS
If a patient presents with a corneal infiltrate but no overlying epithelial staining, the condition is not bacterial keratitis. If there is epithelial breakdown but only minor inflammation and anterior chamber reaction, then it most likely is not infectious bacterial keratitis.
The inflammatory reaction is as damaging to the cornea as the infective organism. Once you've halted bacterial proliferation, be sure to prescribe a steroid to speed healing and reduce corneal scarring. For steroids to be beneficial, they must be used while the ulcer bed is still open, usually within the first 24 to 48 hours. If you wait until the ulcer re-epithelializes before adding a steroid, the beneficial effects will be lost.
The patient will present with a unilateral, acutely painful, photophobic, intensely injected eye. Visual acuity is usually reduced, and profuse tearing is common. There will be a focal stromal infiltrate with an overlying area of epithelial excavation. There is likely to be thick, ropy, mucopurulent discharge.
The cornea will be very edematous. The conjunctival and episcleral vessels will be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal defect. In severe cases, there will be a pronounced anterior chamber reaction, often with hypopyon. Intraocular pressure may be low due to secretory hypotony of the ciliary body, but most often will be elevated due to blockage of the trabecular meshwork by inflammatory cells. Often, the eyelids will also be edematous.
PATHOPHYSIOLOGY
Once the corneal defenses are breached, specifically the epithelial glycocalyx, the cornea is prone to infection. Possible causes include direct corneal trauma, chronic eyelid disease, tear film abnormalities affecting the ocular surface and hypoxic trauma from contact lens wear. Pathogenic bacteria colonize the corneal stroma and immediately become antigenic, both directly and indirectly, by releasing enzymes and toxins.
This sets up an antigen-antibody immune reaction which leads to an inflammatory reaction. The body releases polymorphonuclear leukocytes (PMNs) which aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize and digest the bacteria. The collagen stroma is poorly tolerant of the bacterial and leukocytic enzymes and undergoes degradation, necrosis and thinning. This results in scarring of the cornea. With severe thinning the cornea may perforate, creating the possibility for endophthalmitis.
Throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus aureus. However, in cases involving contact lens wear and cosmetics, the most common infective organism is Pseudomonas aeruginosa.
MANAGEMENT
As with bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting organism but is often difficult or impractical. First and foremost, you must halt bacterial proliferation; do not delay treatment while waiting for the culture results. If you have the materials available, scrape the ulcer using a platinum spatula and plate the specimen onto blood and chocolate agar culture media. A simpler but less effective method is to use a culturette.
Regardless, immediately begin therapy with a broad spectrum antibiotic. A popular initial therapy is the fluoroquinolone ciprofloxacin 0.3% (Ciloxan) two drops every 15 minutes for six hours, followed by two drops every 30 minutes for 18 hours, and then tapered depending on patient response. Another fluoroquinolone, ofloxacin 0.3% (Ocuflox) is also an effective treatment for bacterial keratitis. Both fluoroquinolones are as effective at managing bacterial keratitis as fortified antibiotics, but with significantly fewer side effects.
To increase patient comfort and minimize inflammation, strong cycloplegia is mandatory. Begin with a cycloplegic such as scopolamine 0.25% TID. If this is insufficient, switch to atropine 1% BID. Adjunctive use of cold compresses will also help to reduce inflammation. If there is evidence of secondary inflammatory glaucoma, Rx a topical beta-blocker BID.
Have the patient return daily for follow-up visits. Once the infection is controlled, add a topical steroid Q2H to the regimen. Continue the daily follow-up and begin to taper all medications as you see improvement.
CLINICAL PEARLS
If a patient presents with a corneal infiltrate but no overlying epithelial staining, the condition is not bacterial keratitis. If there is epithelial breakdown but only minor inflammation and anterior chamber reaction, then it most likely is not infectious bacterial keratitis.
The inflammatory reaction is as damaging to the cornea as the infective organism. Once you've halted bacterial proliferation, be sure to prescribe a steroid to speed healing and reduce corneal scarring. For steroids to be beneficial, they must be used while the ulcer bed is still open, usually within the first 24 to 48 hours. If you wait until the ulcer re-epithelializes before adding a steroid, the beneficial effects will be lost.
KERATITIS SICCA / DRY EYE SYNDROME
SIGNS AND SYMPTOMS
As the name implies, patients with keratitis sicca or dry eye syndrome typically present with complaints of dry, burning eyes and a "sandy" or "gritty" foreign body sensation. Occasionally, patients will report excess tearing (epiphora). Often, the symptoms are exacerbated by poor air quality and low humidity, and are more prominent later in the day. Upon inspection, most patients demonstrate a relatively white and quiet eye. Key slit lamp findings include a negligible tear meniscus at the lower lid and a reduced tear break-up time (TBUT), generally less than ten seconds.
Fluorescein staining will usually reveal punctate epithelial keratopathy in the interpalpebral region. In severe cases, the cornea and/or conjunctiva may also stain with rose bengal. Filaments-tags of mucus, epithelial cells and tear debris-may also stain with fluorescein and rose bengal; filamentary keratitis is an extreme sequela of keratitis sicca.
PATHOPHYSIOLOGY
Dry eye syndrome results primarily from compromise to either the quantity or quality of the precorneal tear film. Tears are composed of a mucin layer, a water or aqueous layer, and an oil layer. Deficiencies in any one of these components may create a tear film which is incapable of properly moistening the eye, resulting in desiccation and symptomatic complaints. In addition, irregularities in the blink mechanism or conditions affecting the regularity of the ocular surface (e.g., pterygia, keratoconus) may further interfere with proper wetting of the cornea. Many drugs can also temporarily decrease lacrimal gland secretions, such as antihistamines, phenothiazine anti-anxiety medications, oral contraceptives and atropine derivatives. Collagen vascular disorders such as rheumatoid arthritis and Sjögren's syndrome also have a high association with dry eye syndrome.
MANAGEMENT
Management is aimed at replenishing the eyes' moisture and/or delaying evaporation of the patient's natural tears. Begin by recommending that the patient instill an ophthalmic lubricant every hour or more as needed, then taper the therapy based upon patient response and compliance. A lubricating ointment used at bedtime may provide additional comfort. For those patients who derive little relief from this therapy, or who fail to comply, punctal occlusion may offer a more realistic and less complicated management strategy. First, test the patient's response using dissolvable collagen plugs to ensure the therapy will provide relief from symptoms without epiphora. If successful, occlude the inferior puncta using silicone plugs. In severe cases consider occluding both the inferior and superior puncta, or recommend surgical cautery.
CLINICAL PEARLS
Often, patients with dry eye syndrome are more symptomatic than their clinical signs would imply. Typically, the diagnosis is based more on subjective complaints than slit lamp findings.
Educate patients early and often that dry eye syndrome cannot be cured outright. Rather, the therapy aims to control symptoms and reduce discomfort.
As the name implies, patients with keratitis sicca or dry eye syndrome typically present with complaints of dry, burning eyes and a "sandy" or "gritty" foreign body sensation. Occasionally, patients will report excess tearing (epiphora). Often, the symptoms are exacerbated by poor air quality and low humidity, and are more prominent later in the day. Upon inspection, most patients demonstrate a relatively white and quiet eye. Key slit lamp findings include a negligible tear meniscus at the lower lid and a reduced tear break-up time (TBUT), generally less than ten seconds.
Fluorescein staining will usually reveal punctate epithelial keratopathy in the interpalpebral region. In severe cases, the cornea and/or conjunctiva may also stain with rose bengal. Filaments-tags of mucus, epithelial cells and tear debris-may also stain with fluorescein and rose bengal; filamentary keratitis is an extreme sequela of keratitis sicca.
PATHOPHYSIOLOGY
Dry eye syndrome results primarily from compromise to either the quantity or quality of the precorneal tear film. Tears are composed of a mucin layer, a water or aqueous layer, and an oil layer. Deficiencies in any one of these components may create a tear film which is incapable of properly moistening the eye, resulting in desiccation and symptomatic complaints. In addition, irregularities in the blink mechanism or conditions affecting the regularity of the ocular surface (e.g., pterygia, keratoconus) may further interfere with proper wetting of the cornea. Many drugs can also temporarily decrease lacrimal gland secretions, such as antihistamines, phenothiazine anti-anxiety medications, oral contraceptives and atropine derivatives. Collagen vascular disorders such as rheumatoid arthritis and Sjögren's syndrome also have a high association with dry eye syndrome.
MANAGEMENT
Management is aimed at replenishing the eyes' moisture and/or delaying evaporation of the patient's natural tears. Begin by recommending that the patient instill an ophthalmic lubricant every hour or more as needed, then taper the therapy based upon patient response and compliance. A lubricating ointment used at bedtime may provide additional comfort. For those patients who derive little relief from this therapy, or who fail to comply, punctal occlusion may offer a more realistic and less complicated management strategy. First, test the patient's response using dissolvable collagen plugs to ensure the therapy will provide relief from symptoms without epiphora. If successful, occlude the inferior puncta using silicone plugs. In severe cases consider occluding both the inferior and superior puncta, or recommend surgical cautery.
CLINICAL PEARLS
Often, patients with dry eye syndrome are more symptomatic than their clinical signs would imply. Typically, the diagnosis is based more on subjective complaints than slit lamp findings.
Educate patients early and often that dry eye syndrome cannot be cured outright. Rather, the therapy aims to control symptoms and reduce discomfort.
Giant Papillary Conjunctivitis
Signs and Symptoms
Giant papillary conjunctivitis (GPC) is a common condition frequently seen in soft contact lens patients, patients with exposed suture knots, and patients with prostheses. Patients with asthma, hay fever or animal allergies may be at greater risk. The etiology of GPC may be immunological, where contact lens deposits act as allergens.
Initial presentation may occur months or even years after lens wear has been initiated. The papillae in GPC can be observed on the superior tarsus and (by definition) measure 1mm in diameter. Ocular itching after lens removal, increased mucus discharge in the morning, photophobia and decreased lens tolerance are all initial symptoms. Vision can be affected either as an artifact of the deposits on the lens, due to lens displacement secondary to superior lid papillary hypertrophy, or repetitive mechanical corneal abrasion with infiltration (shield ulceration).
Pathophysiology
The allergic response is considered to be an over-reaction of the body’s immune system to immunogens or allergens. This response can be innate or acquired after multiple exposures to a particular antigen.
The GPC response has no seasonal variation. While the histamine level of tears is increased in vernal keratoconjunctivitis (VKC), it remains level in GPC. Despite this difference, VKC and GPC are pathophysiologically similar. Cytologic scrapings from the conjunctiva of patients with GPC exhibit an immunologic response containing lymphocytes, plasma cells, mast cells, eosinophils and basophils suggesting an antigen-antibody mechanism. The action of phospholipase A2 secondary to the allergic response causes the release of histamines via the degranulation of mast cells. This increases capillary permeability, produces lymphocyte circulation (T-cells, eosinophils, and monocytes) and initiates the liberation of arachidonic acid, which is a catalyst for the cyclooxygenase and lipoxygenase pathways. These pathways produce inflammatory mediators such as thromboxanes, leukotrienes and prostaglandins that cause the discomfort and formation of the papillae.
Management
Management is primarily aimed at reducing symptoms. In more serious cases, aggressive management may be required to prevent ocular tissue damage. The type and frequency of medications depends upon the severity of the condition. Topical supportive therapies act to supplement the biological tears, to wash away debris and environmental allergies. The flushing away of allergens and other debris plays an obvious role in reducing or even canceling the GPC response. Examples of such products include Bion Tears, Tears Naturale Free, Refresh Plus, Ocucoat PF and Dry Eye Therapy.
Topical mast cell stabilizers are a tested and proven modality for treating GPC. Topical mast cell stabilizers are the treatment of choice for chronic GPC. They work by stabilizing the receptors on mast cell vesicles before they can degranulate, beginning the cycle of the allergic response. VKC, atopic keratoconjunctivitis (AKC), and GPC all respond well. If the patient’s history is well known for GPC, a 10-day loading period preceding the onset of symptoms with a preparation like cromolyn sodium (Opticrom, Crolom), at a dosage of four to six times daily, is usually effective in stalling or preventing the initial stages of the disease. Following this, you may need to continue therapy for four to six weeks or until the end of the episode. Another mast cell stabilizer made available in recent years is lodoxamide (Alomide). Like cromolyn sodium, it is a safe drug and is used in the same manner for a wide variety of allergic conditions, at a dosage of two to four times a day. Olopatadine (Patanol) combines mast cell stabilization with antihistamine properties and may be the best therapy due to its dual role. Another advantage of Patanol is its twice daily dosing.
Mast cell stabilizers have been shown to deliver significant therapeutic impact on the GPC reaction. However, to ease chronic irritations of this type, the most effective method remains eradication of the antigen.
In recalcitrant cases, topical corticosteroids function to deliver potent, palliative mediation by reducing the inflammatory response. Topical corticosteroids reduce capillary permeability, suppress lymphocyte circulation, inhibit the degranulation of mast cells, reduce the numbers of basophils and neutrophils, and decrease the production of prostaglandins, thromboxanes and leukotrienes. GPC resistant to standard therapies may respond to topical steroids. Excellent choices of steroids for management of GPC include Vexol, Lotemax, and Alrex.
Clinical Pearls:
Patients with allergic symptoms often have dry eyes as their primary problem. Make sure to rule out tear deficiency in chronic GPC conditions.
When topical steroids are required, you can typically prescribe them four and six times a day for up to seven days to achieve control and then taper off.
The final alternative may entail fitting susceptible patients with daily disposable or rigid gas-permeable lenses, or even discontinuing contact lens wear altogether.
Daily disposable soft contact lenses in combination with medical therapy are an excellent compromise for the patient who absolutely cannot discontinue lens wear for any reason.
Giant papillary conjunctivitis (GPC) is a common condition frequently seen in soft contact lens patients, patients with exposed suture knots, and patients with prostheses. Patients with asthma, hay fever or animal allergies may be at greater risk. The etiology of GPC may be immunological, where contact lens deposits act as allergens.
Initial presentation may occur months or even years after lens wear has been initiated. The papillae in GPC can be observed on the superior tarsus and (by definition) measure 1mm in diameter. Ocular itching after lens removal, increased mucus discharge in the morning, photophobia and decreased lens tolerance are all initial symptoms. Vision can be affected either as an artifact of the deposits on the lens, due to lens displacement secondary to superior lid papillary hypertrophy, or repetitive mechanical corneal abrasion with infiltration (shield ulceration).
Pathophysiology
The allergic response is considered to be an over-reaction of the body’s immune system to immunogens or allergens. This response can be innate or acquired after multiple exposures to a particular antigen.
The GPC response has no seasonal variation. While the histamine level of tears is increased in vernal keratoconjunctivitis (VKC), it remains level in GPC. Despite this difference, VKC and GPC are pathophysiologically similar. Cytologic scrapings from the conjunctiva of patients with GPC exhibit an immunologic response containing lymphocytes, plasma cells, mast cells, eosinophils and basophils suggesting an antigen-antibody mechanism. The action of phospholipase A2 secondary to the allergic response causes the release of histamines via the degranulation of mast cells. This increases capillary permeability, produces lymphocyte circulation (T-cells, eosinophils, and monocytes) and initiates the liberation of arachidonic acid, which is a catalyst for the cyclooxygenase and lipoxygenase pathways. These pathways produce inflammatory mediators such as thromboxanes, leukotrienes and prostaglandins that cause the discomfort and formation of the papillae.
Management
Management is primarily aimed at reducing symptoms. In more serious cases, aggressive management may be required to prevent ocular tissue damage. The type and frequency of medications depends upon the severity of the condition. Topical supportive therapies act to supplement the biological tears, to wash away debris and environmental allergies. The flushing away of allergens and other debris plays an obvious role in reducing or even canceling the GPC response. Examples of such products include Bion Tears, Tears Naturale Free, Refresh Plus, Ocucoat PF and Dry Eye Therapy.
Topical mast cell stabilizers are a tested and proven modality for treating GPC. Topical mast cell stabilizers are the treatment of choice for chronic GPC. They work by stabilizing the receptors on mast cell vesicles before they can degranulate, beginning the cycle of the allergic response. VKC, atopic keratoconjunctivitis (AKC), and GPC all respond well. If the patient’s history is well known for GPC, a 10-day loading period preceding the onset of symptoms with a preparation like cromolyn sodium (Opticrom, Crolom), at a dosage of four to six times daily, is usually effective in stalling or preventing the initial stages of the disease. Following this, you may need to continue therapy for four to six weeks or until the end of the episode. Another mast cell stabilizer made available in recent years is lodoxamide (Alomide). Like cromolyn sodium, it is a safe drug and is used in the same manner for a wide variety of allergic conditions, at a dosage of two to four times a day. Olopatadine (Patanol) combines mast cell stabilization with antihistamine properties and may be the best therapy due to its dual role. Another advantage of Patanol is its twice daily dosing.
Mast cell stabilizers have been shown to deliver significant therapeutic impact on the GPC reaction. However, to ease chronic irritations of this type, the most effective method remains eradication of the antigen.
In recalcitrant cases, topical corticosteroids function to deliver potent, palliative mediation by reducing the inflammatory response. Topical corticosteroids reduce capillary permeability, suppress lymphocyte circulation, inhibit the degranulation of mast cells, reduce the numbers of basophils and neutrophils, and decrease the production of prostaglandins, thromboxanes and leukotrienes. GPC resistant to standard therapies may respond to topical steroids. Excellent choices of steroids for management of GPC include Vexol, Lotemax, and Alrex.
Clinical Pearls:
Patients with allergic symptoms often have dry eyes as their primary problem. Make sure to rule out tear deficiency in chronic GPC conditions.
When topical steroids are required, you can typically prescribe them four and six times a day for up to seven days to achieve control and then taper off.
The final alternative may entail fitting susceptible patients with daily disposable or rigid gas-permeable lenses, or even discontinuing contact lens wear altogether.
Daily disposable soft contact lenses in combination with medical therapy are an excellent compromise for the patient who absolutely cannot discontinue lens wear for any reason.
Thursday, December 23, 2010
Conjunctivitis with Pseudomembrane
Signs and Symptoms
Often, conjunctivitis is discovered by most patients in the morning, when they notice, upon waking, that their eyelids are "stuck together." The classic signs and symptoms of conjunctivitis include ocular redness secondary to palpebral and or bulbar conjunctival injection, irritation, itching, lacrimation, discharge, and possibly keratitis with decreased vision. Conjunctival follicular and papillary response, discharge, subepithelial infiltration, subconjunctival hemorrhage, corneal epitheliopathy, symblepharon formation and lymphadenopathy are variables dictated by the etiology.
Pathophysiology
A true membrane forms when the fibrinous excretory or inflammatory exudate that is secreted by invading microorganisms or ocular tissues permeates the superficial layers of the conjunctival epithelium. True membranes become interdigitated with the vascularity of the conjunctival epithelium. They are firmly adherent, and tearing and bleeding often result when removed. B-hemolytic streptococci, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Stevens-Johnson syndrome (severe systemic vesiculobullous eruptions affecting the mucous membranes-erythema multiforme) and chemical or thermal burns are among the common etiologic sources.
Pseudomembranes consist of coagulated exudate that is loosely adherent to the inflamed conjunctiva. They are typically not integrated with the conjunctival epithelium and can be removed by peeling, leaving the conjunctival epithelium intact. Their removal produces little if any bleeding. Epidemic keratoconjunctivitis (EKC), ligneous conjunctivitis (a rare idiopathic bilateral membranous/pseudomembranous conjunctivitis seen in children with thick, ropy, white discharge on the upper tarsal conjunctiva), allergic conjunctivitis, and bacterial infections are the primary causes.
Epidemic keratoconjunctivitis (EKC) often presents as a bilateral, inferior palpebral, follicular conjunctivitis, with epithelial and subepithelial keratitis and normal corneal sensation. It is extremely contagious. The subepithelial infiltrates (SEI) are typically concentrated in the central cornea. Mild EKC is regularly caused by adenovirus virus serotypes 1, 2, 3, 4. The more severe form of the disease is caused by virus serotypes 5, 8, 19 and 37.
Pharyngoconjunctival fever (PCF) is characterized by history of fever, sore throat, upper respiratory infection, and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and 7. The cornea is rarely affected and infiltrates are uncommon. While the virus is shed from the conjunctiva in 14 days, it remains in fecal excretion for 30 days. This may explain why some epidemics center around swimming pools in summer. The disorder varies in severity and may persist for four days to two weeks.
Management
In most cases, because viral conjunctivitis is contagious and self-limiting, the primary function of management is to increase patient awareness and comfort by providing education and decreasing symptomatology. Patients should be kept home from work or school until contagious discharge is eliminated. Patients should be warned not to use common utensils or linens.
If pseudo- or true membranes are present, debride them using a wet cotton-tipped applicator or forceps. Include supportive therapies such as cold compress and topical tear solutions, topical vasoconstrictors (Naphcon A), topical NSAID preparations (Acular, Voltaren), and topical steroids (Flarex, Pred Forte, Vexol) b.i.d. to q.i.d. Topical antibiotic/steroid combination therapy (Tobradex, Maxitrol) QID is indicated if the infection has a suspected bacterial source. Cycloplegia is only necessary in the most severe cases. When you suspect bacterial etiology, conjunctival scrapings may provide differential diagnostic information.
A new drug is on the horizon for treating entities causing pseudomembraneous conjunctivitis. Cidofovir, a topically applied DNA analog, has been proven clinically efficacious in the treatment of adenoviral conjunctivitis and epidemic keratoconjunctivitis and is currently awaiting approval for commercial use.
Clinical Pearls
The four clinical features that must be considered in the differential diagnosis of any conjunctival inflammation include:r
- Type of discharge (watery, mucoid, purulent, mucopurulent)
- Type of conjunctival reaction (follicular or papillary)
- Presence or absence of membrane or pseudomembrane formation
- Presence or absence of lymphadenopathy (association with sexually transmitted or viral origin)
Epidemic viral conjunctivitis, epidemic keratoconjunctivitis (EKC) and pharyngoconjunctival fever (PCF) can be caused by a number of different viruses and are probably the most common causes of pseudomembranous conjunctivitis.
Often, conjunctivitis is discovered by most patients in the morning, when they notice, upon waking, that their eyelids are "stuck together." The classic signs and symptoms of conjunctivitis include ocular redness secondary to palpebral and or bulbar conjunctival injection, irritation, itching, lacrimation, discharge, and possibly keratitis with decreased vision. Conjunctival follicular and papillary response, discharge, subepithelial infiltration, subconjunctival hemorrhage, corneal epitheliopathy, symblepharon formation and lymphadenopathy are variables dictated by the etiology.
Pathophysiology
A true membrane forms when the fibrinous excretory or inflammatory exudate that is secreted by invading microorganisms or ocular tissues permeates the superficial layers of the conjunctival epithelium. True membranes become interdigitated with the vascularity of the conjunctival epithelium. They are firmly adherent, and tearing and bleeding often result when removed. B-hemolytic streptococci, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Stevens-Johnson syndrome (severe systemic vesiculobullous eruptions affecting the mucous membranes-erythema multiforme) and chemical or thermal burns are among the common etiologic sources.
Pseudomembranes consist of coagulated exudate that is loosely adherent to the inflamed conjunctiva. They are typically not integrated with the conjunctival epithelium and can be removed by peeling, leaving the conjunctival epithelium intact. Their removal produces little if any bleeding. Epidemic keratoconjunctivitis (EKC), ligneous conjunctivitis (a rare idiopathic bilateral membranous/pseudomembranous conjunctivitis seen in children with thick, ropy, white discharge on the upper tarsal conjunctiva), allergic conjunctivitis, and bacterial infections are the primary causes.
Epidemic keratoconjunctivitis (EKC) often presents as a bilateral, inferior palpebral, follicular conjunctivitis, with epithelial and subepithelial keratitis and normal corneal sensation. It is extremely contagious. The subepithelial infiltrates (SEI) are typically concentrated in the central cornea. Mild EKC is regularly caused by adenovirus virus serotypes 1, 2, 3, 4. The more severe form of the disease is caused by virus serotypes 5, 8, 19 and 37.
Pharyngoconjunctival fever (PCF) is characterized by history of fever, sore throat, upper respiratory infection, and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and 7. The cornea is rarely affected and infiltrates are uncommon. While the virus is shed from the conjunctiva in 14 days, it remains in fecal excretion for 30 days. This may explain why some epidemics center around swimming pools in summer. The disorder varies in severity and may persist for four days to two weeks.
Management
In most cases, because viral conjunctivitis is contagious and self-limiting, the primary function of management is to increase patient awareness and comfort by providing education and decreasing symptomatology. Patients should be kept home from work or school until contagious discharge is eliminated. Patients should be warned not to use common utensils or linens.
If pseudo- or true membranes are present, debride them using a wet cotton-tipped applicator or forceps. Include supportive therapies such as cold compress and topical tear solutions, topical vasoconstrictors (Naphcon A), topical NSAID preparations (Acular, Voltaren), and topical steroids (Flarex, Pred Forte, Vexol) b.i.d. to q.i.d. Topical antibiotic/steroid combination therapy (Tobradex, Maxitrol) QID is indicated if the infection has a suspected bacterial source. Cycloplegia is only necessary in the most severe cases. When you suspect bacterial etiology, conjunctival scrapings may provide differential diagnostic information.
A new drug is on the horizon for treating entities causing pseudomembraneous conjunctivitis. Cidofovir, a topically applied DNA analog, has been proven clinically efficacious in the treatment of adenoviral conjunctivitis and epidemic keratoconjunctivitis and is currently awaiting approval for commercial use.
Clinical Pearls
The four clinical features that must be considered in the differential diagnosis of any conjunctival inflammation include:r
- Type of discharge (watery, mucoid, purulent, mucopurulent)
- Type of conjunctival reaction (follicular or papillary)
- Presence or absence of membrane or pseudomembrane formation
- Presence or absence of lymphadenopathy (association with sexually transmitted or viral origin)
Epidemic viral conjunctivitis, epidemic keratoconjunctivitis (EKC) and pharyngoconjunctival fever (PCF) can be caused by a number of different viruses and are probably the most common causes of pseudomembranous conjunctivitis.
Toxic Conjunctivitis
Signs and Symptoms
Toxic conjunctivitis, sometimes referred to as toxic follicular conjunctivitis, is a syndrome that results when the palpebral and bulbar conjunctiva have been chronically exposed to any number or combinations of foreign substances. The process may occur unilaterally or bilaterally, depending upon exposure. Its clinical features include the presentation of ocular itching, burning and tearing, injection of the bulbar and palpebral conjunctivae, chemosis, along with inferior and or superior eyelid follicle and papillae formation, and an absence of preauricular lymphadenopathy. Keratopathy is often present secondarily. In chronic cases, pannus formation may result.
Typically, patients present with a history of using or starting an ocular medication for an episode of presumed bacterial or viral conjunctivitis only to find that the ocular symptoms and signs continue to increase despite correct usage of the medicine. The term medicamentosa is applicable here; it connotes a reaction to the preservatives in medications, or the medications themselves, producing a more substantial keratitis.
Pathophysiology
The toxic/allergic response is an over-reaction of the body’s immune system to immunogens or allergens. The response can be innate or acquired. A variation of this over-reaction is manifested when the body responds hyperactively to exogenous materials such as medicines, contact lenses, contact lens solutions, dust, dander or viral shedding. Overactivity of this type is commonly referred to as a toxic or allergic reaction. With respect to the eye and its adnexa, the result is toxic conjunctivitis.
The key component to the ocular allergic response is the mast cell. When mast cells interact with specific allergens, like a lock being opened by a key, they open (degranulation) discharging chemical mediators into the surrounding tissues. The primary chemical mediators include histamine (responsible for increased vascular permeability, vasodilation, bronchial constriction and increased secretion of mucous), neutral proteases (generating other inflammatory mediators) and arachidonic acid (crucial component of the cyclooxygenase pathway leading to production of prostaglandins and leukotrienes).
There are four types of hypersensitivity reactions.
Type I reactions are immediate hypersensitivity reactions or anaphylactic reactions. These reactions produce sudden degranulation of mast cells mediated by the antibody IgE.
Type II reactions involve the body’s ability to distinguish itself from non-self. Abnormalities in this element of the system give rise to autoimmune disease.
Type III reactions involve combinations of antigen and antibody known as immune complexes. Offending triggers may be intrinsic (i.e. a protein molecule) or extrinsic (a penicillin molecule) and produce a significant tissue response in an attempt to rid the area of the invader.
Type IV reactions, sometimes referred to as cell mediated hypersensitivity reactions, involve the T-lymphocytes and lymphokines. The reaction is classically delayed until sufficient antigens stimulate the chemical cascade. In the ocular tissues, these chemical exchanges incite conjunctival and adnexal vasodilation, chemosis, edema and lacrimation. Individuals experience pain, itching, swelling and irritation. The discharge produced is typically serous and the conjunctival findings include follicles (hyperplasia of lymphoid tissue within the eyelid stroma) and papillae (hyperplastic palpebral conjunctival epithelium infiltrated by lymphocytes and plasma cells).
Management
Management is primarily aimed at reducing symptomatology. Cold compress, artificial tear drops and ointments soothe and lubricate. Topical decongestants produce vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release of the chemical mediators into the tissues from the blood stream. Topical antihistamines (Emadine, Livostin, b.i.d. to q.i.d.) and oral antihistamines (Benadryl, 25 to 50mg, p.o. t.i.d.) are also excellent therapies for acute signs and symptoms. Mast cell stabilizers such as cromolyn sodium (Opticrom) and lodoxamide tromethamine (Alomide) may be useful in seasonal or chronic cases. The non-steroidal anti-inflammatory drugs (NSAIDS: Acular, Voltaren, b.i.d. to q.i.d.) may offer relief in moderate cases, while topical steroid preparations (Alrex, Lotemax, FML, FML Forte, Allergan, Pred Mild, Pred Forte, Flarex, Vexol, b.i.d. to q.i.d., and Inflamase Mild and Forte, b.i.d. to q.i.d.) are reserved for the most symptomatic presentations.
Clinical Pearls
Toxic/allergic conjunctivitis is a diagnosis that can be made based upon history and course. Typically, vision is unaffected despite its unruly appearance. You can usually identify a causative source as the precipitator of the acute signs and symptoms. Even if left untreated, toxic conjunctivitis often begins to resolve within seven days.
In true toxic conjunctivitis, there will not be a palpable preauricular lymph node.
Toxic conjunctivitis, sometimes referred to as toxic follicular conjunctivitis, is a syndrome that results when the palpebral and bulbar conjunctiva have been chronically exposed to any number or combinations of foreign substances. The process may occur unilaterally or bilaterally, depending upon exposure. Its clinical features include the presentation of ocular itching, burning and tearing, injection of the bulbar and palpebral conjunctivae, chemosis, along with inferior and or superior eyelid follicle and papillae formation, and an absence of preauricular lymphadenopathy. Keratopathy is often present secondarily. In chronic cases, pannus formation may result.
Typically, patients present with a history of using or starting an ocular medication for an episode of presumed bacterial or viral conjunctivitis only to find that the ocular symptoms and signs continue to increase despite correct usage of the medicine. The term medicamentosa is applicable here; it connotes a reaction to the preservatives in medications, or the medications themselves, producing a more substantial keratitis.
Pathophysiology
The toxic/allergic response is an over-reaction of the body’s immune system to immunogens or allergens. The response can be innate or acquired. A variation of this over-reaction is manifested when the body responds hyperactively to exogenous materials such as medicines, contact lenses, contact lens solutions, dust, dander or viral shedding. Overactivity of this type is commonly referred to as a toxic or allergic reaction. With respect to the eye and its adnexa, the result is toxic conjunctivitis.
The key component to the ocular allergic response is the mast cell. When mast cells interact with specific allergens, like a lock being opened by a key, they open (degranulation) discharging chemical mediators into the surrounding tissues. The primary chemical mediators include histamine (responsible for increased vascular permeability, vasodilation, bronchial constriction and increased secretion of mucous), neutral proteases (generating other inflammatory mediators) and arachidonic acid (crucial component of the cyclooxygenase pathway leading to production of prostaglandins and leukotrienes).
There are four types of hypersensitivity reactions.
Type I reactions are immediate hypersensitivity reactions or anaphylactic reactions. These reactions produce sudden degranulation of mast cells mediated by the antibody IgE.
Type II reactions involve the body’s ability to distinguish itself from non-self. Abnormalities in this element of the system give rise to autoimmune disease.
Type III reactions involve combinations of antigen and antibody known as immune complexes. Offending triggers may be intrinsic (i.e. a protein molecule) or extrinsic (a penicillin molecule) and produce a significant tissue response in an attempt to rid the area of the invader.
Type IV reactions, sometimes referred to as cell mediated hypersensitivity reactions, involve the T-lymphocytes and lymphokines. The reaction is classically delayed until sufficient antigens stimulate the chemical cascade. In the ocular tissues, these chemical exchanges incite conjunctival and adnexal vasodilation, chemosis, edema and lacrimation. Individuals experience pain, itching, swelling and irritation. The discharge produced is typically serous and the conjunctival findings include follicles (hyperplasia of lymphoid tissue within the eyelid stroma) and papillae (hyperplastic palpebral conjunctival epithelium infiltrated by lymphocytes and plasma cells).
Management
Management is primarily aimed at reducing symptomatology. Cold compress, artificial tear drops and ointments soothe and lubricate. Topical decongestants produce vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release of the chemical mediators into the tissues from the blood stream. Topical antihistamines (Emadine, Livostin, b.i.d. to q.i.d.) and oral antihistamines (Benadryl, 25 to 50mg, p.o. t.i.d.) are also excellent therapies for acute signs and symptoms. Mast cell stabilizers such as cromolyn sodium (Opticrom) and lodoxamide tromethamine (Alomide) may be useful in seasonal or chronic cases. The non-steroidal anti-inflammatory drugs (NSAIDS: Acular, Voltaren, b.i.d. to q.i.d.) may offer relief in moderate cases, while topical steroid preparations (Alrex, Lotemax, FML, FML Forte, Allergan, Pred Mild, Pred Forte, Flarex, Vexol, b.i.d. to q.i.d., and Inflamase Mild and Forte, b.i.d. to q.i.d.) are reserved for the most symptomatic presentations.
Clinical Pearls
Toxic/allergic conjunctivitis is a diagnosis that can be made based upon history and course. Typically, vision is unaffected despite its unruly appearance. You can usually identify a causative source as the precipitator of the acute signs and symptoms. Even if left untreated, toxic conjunctivitis often begins to resolve within seven days.
In true toxic conjunctivitis, there will not be a palpable preauricular lymph node.
Superior Limbic Keratoconjunctivitis (SLK of Theodore)
Signs and Symptoms
Individuals presenting with SLK typically report symptoms of ocular discomfort, including burning, foreign-body sensation, or non-descript pain. Additionally, patients may complain of photophobia and excessive tearing. Gross clinical signs often include mild lid swelling and pseudoptosis as well as blepharospasm. Visual acuity is usually not affected.
Inspection of the ocular surface in SLK reveals a sectoral inflammation and injection of the superior bulbar conjunctiva. The limbal margin of the cornea may be inflamed as well. Eversion of the upper lid reveals a uniform papillary hypertrophy along the tarsus, which may be mild to marked. Vital dye staining is standard in SLK, with patients displaying punctate epithelial disruption of the affected region; this is evident with both sodium fluorescein dye as well as rose bengal or lissamine green solutions. Filaments are encountered within the precorneal tear film in roughly half of all patients with SLK. The condition is typically bilateral but often asymmetric. In most instances, the diagnosis of SLK is based solely upon the characteristic presentation. The only known laboratory confirmation is the presence of keratinized epithelial cells from scrapings of the affected superior bulbar conjunctivae.
Pathophysiology
The exact etiology and pathogenesis of SLK remains unclear. Infectious agents such as bacteria, viruses, fungi, and other intracellular parasites appear to be unrelated to this condition. An autoimmune etiology has been considered, based upon the pattern of the disorder (i.e., exacerbations and remissions), the female predominance, and an association with thyroid disease and other autoimmune diseases.
The most widely accepted theory regarding the pathogenesis of SLK is that it results from mechanical irritation of the superior limbal region, as loose conjunctival tissue rubs against the limbus during blinking. Factors such as tight lids, prominent globes, and thyroid disease have been offered as potential instigators of this reaction.
A newer theory regarding the etiology of SLK implicates a local tear deficiency to the superior keratoconjunctiva. Researchers have proposed that this deficiency results in significantly reduced levels of vital tear-based nutrients to the affected region, as well as increased mechanical friction from the superior lid.
Management
SLK is a chronic, recurrent and sometimes recalcitrant disorder. While no treatment has yet been shown to be 100 percent effective, many modalities have been employed successfully. The treatment of choice for most practitioners has been 0.5 to 1.0% silver nitrate solution, applied topically to the superior bulbar and tarsal conjunctivae. This treatment chemically cauterizes the irregular tissue, promoting regrowth of new, healthy epithelium. Unfortunately, recurrences have been known to occur after using silver nitrate, and retreatments are common.
Pressure patching has been employed for severely symptomatic cases of SLK, as well as the use of subsequent bandage hydrogel lenses to alleviate the mechanical irritation. Thermal cauterization as well as surgical recession or resection of the superior bulbar conjunctiva has also been employed as treatment modalities for SLK. The use of topical preparations, including vitamin A eyedrops, 4% cromolyn sodium solution, and Alomide (0.1% lodoxamide tromethamine solution, Alcon) have also been somewhat effective in managing SLK. Most recently, lacrimal punctal occlusion therapy has been advocated for this disorder.
Clinical Pearls
In managing this disorder, topical agents should be employed in the early stages of all mild and moderate presentations; thermocautery, chemocautery, and surgical resection should be employed only when less invasive means have failed.
Lacrimal occlusion therapy may prove to be a viable option for SLK; while additional research is needed in this area, recent studies have shown great potential.
SLK of Theodore should not be confused with contact lens-induced SLK (CL-SLK), a condition that is occasionally observed in young, otherwise healthy hydrogel lens wearers. An association with thimerosal-preserved solutions has been seen in some of these patients. The typical presentation of CL-SLK consists of increasing contact lens intolerance, superior tarsal and bulbar injection, and significant superior corneal staining with stromal hazing. Corneal involvement may be noted as far inferiorly as the superior pupillary margin. Treatment for CL-SLK consists of temporarily discontinuing contact lens wear, along with the liberal use of preservative-free ocular lubricants. Upon resolution, contact lens wear may be resumed with a fresh pair of lenses, however all thimerosal-preserved solutions should be terminated. In more severe or recurrent cases, patients may need to be refit with RGP materials.
Refer all patients presenting with SLK for a systemic workup, including a serologic thyroid panel. A 1995 study demonstrated a 65 percent correlation between SLK and systemic thyroid disease. Other disorders such as rheumatoid arthritis and Sjögren’s syndrome may also have similar associations.
Individuals presenting with SLK typically report symptoms of ocular discomfort, including burning, foreign-body sensation, or non-descript pain. Additionally, patients may complain of photophobia and excessive tearing. Gross clinical signs often include mild lid swelling and pseudoptosis as well as blepharospasm. Visual acuity is usually not affected.
Inspection of the ocular surface in SLK reveals a sectoral inflammation and injection of the superior bulbar conjunctiva. The limbal margin of the cornea may be inflamed as well. Eversion of the upper lid reveals a uniform papillary hypertrophy along the tarsus, which may be mild to marked. Vital dye staining is standard in SLK, with patients displaying punctate epithelial disruption of the affected region; this is evident with both sodium fluorescein dye as well as rose bengal or lissamine green solutions. Filaments are encountered within the precorneal tear film in roughly half of all patients with SLK. The condition is typically bilateral but often asymmetric. In most instances, the diagnosis of SLK is based solely upon the characteristic presentation. The only known laboratory confirmation is the presence of keratinized epithelial cells from scrapings of the affected superior bulbar conjunctivae.
Pathophysiology
The exact etiology and pathogenesis of SLK remains unclear. Infectious agents such as bacteria, viruses, fungi, and other intracellular parasites appear to be unrelated to this condition. An autoimmune etiology has been considered, based upon the pattern of the disorder (i.e., exacerbations and remissions), the female predominance, and an association with thyroid disease and other autoimmune diseases.
The most widely accepted theory regarding the pathogenesis of SLK is that it results from mechanical irritation of the superior limbal region, as loose conjunctival tissue rubs against the limbus during blinking. Factors such as tight lids, prominent globes, and thyroid disease have been offered as potential instigators of this reaction.
A newer theory regarding the etiology of SLK implicates a local tear deficiency to the superior keratoconjunctiva. Researchers have proposed that this deficiency results in significantly reduced levels of vital tear-based nutrients to the affected region, as well as increased mechanical friction from the superior lid.
Management
SLK is a chronic, recurrent and sometimes recalcitrant disorder. While no treatment has yet been shown to be 100 percent effective, many modalities have been employed successfully. The treatment of choice for most practitioners has been 0.5 to 1.0% silver nitrate solution, applied topically to the superior bulbar and tarsal conjunctivae. This treatment chemically cauterizes the irregular tissue, promoting regrowth of new, healthy epithelium. Unfortunately, recurrences have been known to occur after using silver nitrate, and retreatments are common.
Pressure patching has been employed for severely symptomatic cases of SLK, as well as the use of subsequent bandage hydrogel lenses to alleviate the mechanical irritation. Thermal cauterization as well as surgical recession or resection of the superior bulbar conjunctiva has also been employed as treatment modalities for SLK. The use of topical preparations, including vitamin A eyedrops, 4% cromolyn sodium solution, and Alomide (0.1% lodoxamide tromethamine solution, Alcon) have also been somewhat effective in managing SLK. Most recently, lacrimal punctal occlusion therapy has been advocated for this disorder.
Clinical Pearls
In managing this disorder, topical agents should be employed in the early stages of all mild and moderate presentations; thermocautery, chemocautery, and surgical resection should be employed only when less invasive means have failed.
Lacrimal occlusion therapy may prove to be a viable option for SLK; while additional research is needed in this area, recent studies have shown great potential.
SLK of Theodore should not be confused with contact lens-induced SLK (CL-SLK), a condition that is occasionally observed in young, otherwise healthy hydrogel lens wearers. An association with thimerosal-preserved solutions has been seen in some of these patients. The typical presentation of CL-SLK consists of increasing contact lens intolerance, superior tarsal and bulbar injection, and significant superior corneal staining with stromal hazing. Corneal involvement may be noted as far inferiorly as the superior pupillary margin. Treatment for CL-SLK consists of temporarily discontinuing contact lens wear, along with the liberal use of preservative-free ocular lubricants. Upon resolution, contact lens wear may be resumed with a fresh pair of lenses, however all thimerosal-preserved solutions should be terminated. In more severe or recurrent cases, patients may need to be refit with RGP materials.
Refer all patients presenting with SLK for a systemic workup, including a serologic thyroid panel. A 1995 study demonstrated a 65 percent correlation between SLK and systemic thyroid disease. Other disorders such as rheumatoid arthritis and Sjögren’s syndrome may also have similar associations.
Pterygium
SIGNS AND SYMPTOMS
In most cases, routine ocular evaluation reveals pterygia in asymptomatic individuals or in patients who present with cosmetic concern about a tissue "growing over the eye." In some instances, the vascularized pterygium may become red and inflamed, motivating the patient to seek immediate care. In other cases, the irregular ocular surface can interfere with the stability of the precorneal tear film, creating a symptomatic dry eye syndrome. Rarely, the pterygium may induce irregular corneal warpage, or even obscure the visual axis of the eye, resulting in diminished acuity.
Clinical inspection of pterygia reveals a raised, whitish, triangular wedge of fibrovascular tissue, whose base lies within the interpalpebral conjunctiva and whose apex encroaches the cornea. The leading edge of this tissue often displays a fine, reddish-brown iron deposition line (Stocker's line).
The vast majority of pterygia (about 90 percent) are located nasally. These lesions are more commonly encountered in warm, dry climates, or in patients who are chronically exposed to outdoor elements or smoky/dusty environments.
Pterygia must be distinguished from pingueculae, which are more yellow in color and lie within the interpalpebral space but generally do not encroach beyond the limbus. Pingueculae also lack the wing-shaped appearance of pterygia, the former being more oval or ameboid in appearance.
PATHOPHYSIOLOGY
Ultraviolet light exposure (both UV-A and UV-B) appears to be the most significant factor in the development of pterygia. This may explain why the incidence is vastly greater in populations near the equator and in persons who spend a great deal of time outdoors. Other agents that may contribute to the formation of pterygia include allergens, noxious chemicals and irritants (e.g., wind, dirt, dust, air pollution). Heredity may also be a factor.
Whatever the etiology, pterygia represent a degeneration of the conjunctival stroma with replacement by thickened, tortuous elastotic fibers. Activated fibroblasts in the leading edge of the pterygium invade and fragment Bowman's layer as well as a variable amount of the superficial corneal stroma. Histologically, pterygium development resembles actinic degeneration of the skin.
Pterygia often persist after surgical removal; these lesions appear as a fibrovascular scar arising from the excision site. These "recurrent pterygia" probably have no relationship to ultraviolet radiation, but rather may be likened to keloid development in the skin.
MANAGEMENT
Because pterygia appear to be linked to environmental exposure, manage asymptomatic or mildly irritative cases with UV-blocking spectacles and liberal ocular lubrication. Advise patients to avoid smoky or dusty areas as much as possible. Treat more inflamed or irritated pterygia with topical decongestant/antihistamine combinations (e.g., Naphcon-A) and/or mild topical corticosteroids (e.g., FML, Vexol) four times daily in the affected eye.
Surgical excision of pterygia is indicated only for unacceptable cosmesis and/or significant encroachment of the visual axis. The treatment of choice involves dissection and removal of the fibrous tissue down to the level of Tenon's capsule. Free conjunctival flaps are then grafted over the bare sclera. Postoperative adjuvant therapy with b-radiation, topical thiotepa, mitomycin-C and other antimetabolic agents may diminish the chance of recurrence. In cases that involve significant corneal scarring, lamellar or penetrating keratoplasty may be indicated.
CLINICAL PEARLS
A pterygium is a benign clinical entity in most cases. Distinguish between the potentially progressive pterygium and the less threatening pinguecula-large pingueculae may be difficult to differentiate from pterygia.
Conjunctival intraepithelial neoplasia (CIN), a precursor of conjunctival squamous cell carcinoma, is another clinical entity that must be ruled out in the diagnosis of pterygia. This lesion is generally unilateral, elevated and gelatinous, with deep irregular vascularization and an ameboid shape. CIN is an invasive ocular cancer that can inflict significant morbidity. Obtain a biopsy if CIN is suspected.
Pterygia can affect vision if left unchecked. The corneal degradation may extend beyond the leading edge of the lesion. This means that the pterygium need not cover the visual axis to inflict significant visual compromise. Surgery must be performed before vision is affected.
Follow up on medium- to large-sized pterygia at least once or twice yearly, and include a manifest refraction, corneal topography, slit lamp evaluation with measurement of the pterygium, and photodocumentation if possible.
In most cases, routine ocular evaluation reveals pterygia in asymptomatic individuals or in patients who present with cosmetic concern about a tissue "growing over the eye." In some instances, the vascularized pterygium may become red and inflamed, motivating the patient to seek immediate care. In other cases, the irregular ocular surface can interfere with the stability of the precorneal tear film, creating a symptomatic dry eye syndrome. Rarely, the pterygium may induce irregular corneal warpage, or even obscure the visual axis of the eye, resulting in diminished acuity.
Clinical inspection of pterygia reveals a raised, whitish, triangular wedge of fibrovascular tissue, whose base lies within the interpalpebral conjunctiva and whose apex encroaches the cornea. The leading edge of this tissue often displays a fine, reddish-brown iron deposition line (Stocker's line).
The vast majority of pterygia (about 90 percent) are located nasally. These lesions are more commonly encountered in warm, dry climates, or in patients who are chronically exposed to outdoor elements or smoky/dusty environments.
Pterygia must be distinguished from pingueculae, which are more yellow in color and lie within the interpalpebral space but generally do not encroach beyond the limbus. Pingueculae also lack the wing-shaped appearance of pterygia, the former being more oval or ameboid in appearance.
PATHOPHYSIOLOGY
Ultraviolet light exposure (both UV-A and UV-B) appears to be the most significant factor in the development of pterygia. This may explain why the incidence is vastly greater in populations near the equator and in persons who spend a great deal of time outdoors. Other agents that may contribute to the formation of pterygia include allergens, noxious chemicals and irritants (e.g., wind, dirt, dust, air pollution). Heredity may also be a factor.
Whatever the etiology, pterygia represent a degeneration of the conjunctival stroma with replacement by thickened, tortuous elastotic fibers. Activated fibroblasts in the leading edge of the pterygium invade and fragment Bowman's layer as well as a variable amount of the superficial corneal stroma. Histologically, pterygium development resembles actinic degeneration of the skin.
Pterygia often persist after surgical removal; these lesions appear as a fibrovascular scar arising from the excision site. These "recurrent pterygia" probably have no relationship to ultraviolet radiation, but rather may be likened to keloid development in the skin.
MANAGEMENT
Because pterygia appear to be linked to environmental exposure, manage asymptomatic or mildly irritative cases with UV-blocking spectacles and liberal ocular lubrication. Advise patients to avoid smoky or dusty areas as much as possible. Treat more inflamed or irritated pterygia with topical decongestant/antihistamine combinations (e.g., Naphcon-A) and/or mild topical corticosteroids (e.g., FML, Vexol) four times daily in the affected eye.
Surgical excision of pterygia is indicated only for unacceptable cosmesis and/or significant encroachment of the visual axis. The treatment of choice involves dissection and removal of the fibrous tissue down to the level of Tenon's capsule. Free conjunctival flaps are then grafted over the bare sclera. Postoperative adjuvant therapy with b-radiation, topical thiotepa, mitomycin-C and other antimetabolic agents may diminish the chance of recurrence. In cases that involve significant corneal scarring, lamellar or penetrating keratoplasty may be indicated.
CLINICAL PEARLS
A pterygium is a benign clinical entity in most cases. Distinguish between the potentially progressive pterygium and the less threatening pinguecula-large pingueculae may be difficult to differentiate from pterygia.
Conjunctival intraepithelial neoplasia (CIN), a precursor of conjunctival squamous cell carcinoma, is another clinical entity that must be ruled out in the diagnosis of pterygia. This lesion is generally unilateral, elevated and gelatinous, with deep irregular vascularization and an ameboid shape. CIN is an invasive ocular cancer that can inflict significant morbidity. Obtain a biopsy if CIN is suspected.
Pterygia can affect vision if left unchecked. The corneal degradation may extend beyond the leading edge of the lesion. This means that the pterygium need not cover the visual axis to inflict significant visual compromise. Surgery must be performed before vision is affected.
Follow up on medium- to large-sized pterygia at least once or twice yearly, and include a manifest refraction, corneal topography, slit lamp evaluation with measurement of the pterygium, and photodocumentation if possible.
Pingueculitis
SIGNS AND SYMPTOMS
Pingueculae are characterized by yellowish, slightly raised, interpalpebral lipid-like deposits in the nasal and temporal limbal conjunctiva. They are found frequently in individuals who are middle-aged and who experience chronic exposure to the sun. There is no predilection for sex or race.
In most cases, pingueculae are an ancillary finding, causing little, if any, ocular symptoms. Frequently, pingueculae can lead to the formation of pterygia. Both pingueculae and pterygia can become vascularized and inflamed, and may be associated with corneal punctate epitheliopathy and corneal dellen (corneal thinning secondary to dryness).
Pingueculitis occurs when a pinguecula becomes acutely inflamed, vascularized, red, irritated and highly symptomatic.
PATHOPHYSIOLOGY
Pinguecula formation is typically seen in the older population and is considered by most researchers to be a conjunctival degenerative processes initiated by exposure to noxious environmental stimuli and UV light. The initial lesion is thought to result from chronic solar radiation, which alters the collagen and elastic tissues of the conjunctival stroma and leads to elastotic degeneration and deposition of abnormal elastic fibers in the conjunctival substantia propria.
Once a pinguecular elevation forms-depending on its size-the tear film may become thin and discontinuous in that zone, producing a bed of dryness. When the lesion is inflamed, vascular dilation allows the release of histamine, seratonin, bradykinin and prostaglandins, producing the acute irritation that characterize pingueculitis. In severe cases the conjunctival surface becomes sufficiently dry to cause microulceration of the conjunctival epithelium. When this occurs, the eye protects itself by attempting to cover the erosion, leading to pterygium formation.
MANAGEMENT
Manage pinguecula based on symptomatology. For patients with occupations or hobbies that increase the risk of pinguecula, counsel them on the preventative benefits of sunwear, UV-blocking coatings or goggles that limit dust exposure.
In cases of mild pingueculitis, where symptoms are mild or when dellen are present, use ocular lubricating drops such as Tears Naturale II or ointments such as Refresh PM or Lacrilube. When symptoms and inflammation become significant, appropriate topical steroids, used Q2H to QID, include fluorometholone 0.25% (Flarex), 1% rimexolone acetate (Vexol), 0.12% prednisolone acetate suspension (Pred Mild), 0.12% prednisolone sodium phosphate solution (Inflamase Mild), 1% prednisolone acetate suspension (Pred Forte) 1% prednisolone sodium phosphate solution (Inflamase Forte).
Consider surgical resection in severe cases where pterygia are present and are interfering with vision, contact lens wear or corneal wetting.
CLINICAL PEARLS
If you discover an intrapalpebral conjunctival mass or elevation, consider the differential diagnosis. Lesions such as these are not all benign, and include conjunctival dermoid (a white mass seen in Goldenhar's syndrome), cancerous or precancerous conjunctival intraepithelial neoplasia (a unilateral, white, vascularized mass), phlyctenulosis (a white, steep mass associated with Staphylococcus hypersensitivity and tuberculosis), pannus (a fibrovascular conjunctival growth on the cornea associated with severe dry eye, chlamydial infection, chemical or thermal injury), conjunctival retention cyst (a clear, fluid-filled sac) and limbal follicle.
Pingueculae are characterized by yellowish, slightly raised, interpalpebral lipid-like deposits in the nasal and temporal limbal conjunctiva. They are found frequently in individuals who are middle-aged and who experience chronic exposure to the sun. There is no predilection for sex or race.
In most cases, pingueculae are an ancillary finding, causing little, if any, ocular symptoms. Frequently, pingueculae can lead to the formation of pterygia. Both pingueculae and pterygia can become vascularized and inflamed, and may be associated with corneal punctate epitheliopathy and corneal dellen (corneal thinning secondary to dryness).
Pingueculitis occurs when a pinguecula becomes acutely inflamed, vascularized, red, irritated and highly symptomatic.
PATHOPHYSIOLOGY
Pinguecula formation is typically seen in the older population and is considered by most researchers to be a conjunctival degenerative processes initiated by exposure to noxious environmental stimuli and UV light. The initial lesion is thought to result from chronic solar radiation, which alters the collagen and elastic tissues of the conjunctival stroma and leads to elastotic degeneration and deposition of abnormal elastic fibers in the conjunctival substantia propria.
Once a pinguecular elevation forms-depending on its size-the tear film may become thin and discontinuous in that zone, producing a bed of dryness. When the lesion is inflamed, vascular dilation allows the release of histamine, seratonin, bradykinin and prostaglandins, producing the acute irritation that characterize pingueculitis. In severe cases the conjunctival surface becomes sufficiently dry to cause microulceration of the conjunctival epithelium. When this occurs, the eye protects itself by attempting to cover the erosion, leading to pterygium formation.
MANAGEMENT
Manage pinguecula based on symptomatology. For patients with occupations or hobbies that increase the risk of pinguecula, counsel them on the preventative benefits of sunwear, UV-blocking coatings or goggles that limit dust exposure.
In cases of mild pingueculitis, where symptoms are mild or when dellen are present, use ocular lubricating drops such as Tears Naturale II or ointments such as Refresh PM or Lacrilube. When symptoms and inflammation become significant, appropriate topical steroids, used Q2H to QID, include fluorometholone 0.25% (Flarex), 1% rimexolone acetate (Vexol), 0.12% prednisolone acetate suspension (Pred Mild), 0.12% prednisolone sodium phosphate solution (Inflamase Mild), 1% prednisolone acetate suspension (Pred Forte) 1% prednisolone sodium phosphate solution (Inflamase Forte).
Consider surgical resection in severe cases where pterygia are present and are interfering with vision, contact lens wear or corneal wetting.
CLINICAL PEARLS
If you discover an intrapalpebral conjunctival mass or elevation, consider the differential diagnosis. Lesions such as these are not all benign, and include conjunctival dermoid (a white mass seen in Goldenhar's syndrome), cancerous or precancerous conjunctival intraepithelial neoplasia (a unilateral, white, vascularized mass), phlyctenulosis (a white, steep mass associated with Staphylococcus hypersensitivity and tuberculosis), pannus (a fibrovascular conjunctival growth on the cornea associated with severe dry eye, chlamydial infection, chemical or thermal injury), conjunctival retention cyst (a clear, fluid-filled sac) and limbal follicle.
Scleritis
SIGNS AND SYMPTOMS
Unlike the mild sensitivity of episcleritis, true scleritis presents with severe, boring ocular pain which may also involve the adjacent head and facial regions. The scleral vessels are significantly dilated, as are the overlying vessels of the episclera and bulbar conjunctiva. The affected eye may be so injected in some cases that the eye actually takes on a deep red, almost purple, hue. This presentation may be sectoral or diffuse.
Patients typically report a gradual onset of the pain and redness, with associated photophobia, tearing and decreased vision. Slip lamp evaluation may reveal scleral nodules (nodular scleritis), peripheral keratitis and secondary uveitis in some instances. In severe cases of necrotizing scleritis, the sclera may become transparent due to chronic inflammation, revealing the underlying dark blue of the choroid.
PATHOPHYSIOLOGY
Scleritis is a primary inflammation of the sclera, which is often (over 50 percent of cases) associated with systemic disease. Among the most common related disorders are rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, polyarteritis nodosa, Wegener's granulomatosis, herpes zoster virus, gout and syphilis.
Unlike episcleritis, the inflammation characteristic of scleritis has the capacity to spread to other ocular tissues of the anterior segment and/or posterior segment. Consequently, if you do not begin treatment of scleritis immediately, the condition poses the risk of severe visual compromise in the form of cataracts, secondary glaucoma, choroidal or exudative retinal detachment or optic atrophy.
MANAGEMENT
Topical medications alone are generally insufficient in managing scleritis. In addition to cycloplegia (scopolamine 0.25% BID/QID or atropine 1% BID) and a topical steroid, scleritis indicates a systemic anti-inflammatory agents as well. Treat moderate sectoral or diffuse anterior scleritis with oral NSAIDs (e.g., ibuprofen 600mg QID or indomethacin 25mg TID).
If the inflammation is severe or necrotizing, or if non-steroidals alone fail to suppress the inflammation, use a systemic steroid such as oral prednisone 80mg QD for two to three days, then slowly taper to 10 to 20mg daily. It may also be necessary for patients to receive a small maintenance dose for up to one month to control the condition. In rare cases, the patient may require immunosuppressive agents and should be managed by a rheumatologist.
CLINICAL PEARLS
Treated improperly, scleritis can render a great deal of damage to the affected eye.
Be sure to distinguish between this disorder and the less threatening episcleritis.
Occasionally, an atypical presentation of necrotizing scleritis without inflammation may occur; this is known as scleromalacia perforans. In this presentation, the sclera thins significantly in discrete areas, allowing for local outpouchings of the underlying choroid. There is no recognized treatment for this condition.
In all cases of scleritis, always consider the underlying cause to be systemic disease until proven otherwise. Refer patients for a comprehensive medical evaluation, including serology and radiology studies where appropriate. Specific tests may include: complete blood count (CBC) with differential, erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), HLA-B27, rheumatoid factor (RF), angiotensin-converting enzyme (ACE), fluorescent treponemal antibody absorption (FTA-ABS), lyme titer, chest X-ray and sacroiliac joint films.
Unlike the mild sensitivity of episcleritis, true scleritis presents with severe, boring ocular pain which may also involve the adjacent head and facial regions. The scleral vessels are significantly dilated, as are the overlying vessels of the episclera and bulbar conjunctiva. The affected eye may be so injected in some cases that the eye actually takes on a deep red, almost purple, hue. This presentation may be sectoral or diffuse.
Patients typically report a gradual onset of the pain and redness, with associated photophobia, tearing and decreased vision. Slip lamp evaluation may reveal scleral nodules (nodular scleritis), peripheral keratitis and secondary uveitis in some instances. In severe cases of necrotizing scleritis, the sclera may become transparent due to chronic inflammation, revealing the underlying dark blue of the choroid.
PATHOPHYSIOLOGY
Scleritis is a primary inflammation of the sclera, which is often (over 50 percent of cases) associated with systemic disease. Among the most common related disorders are rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, polyarteritis nodosa, Wegener's granulomatosis, herpes zoster virus, gout and syphilis.
Unlike episcleritis, the inflammation characteristic of scleritis has the capacity to spread to other ocular tissues of the anterior segment and/or posterior segment. Consequently, if you do not begin treatment of scleritis immediately, the condition poses the risk of severe visual compromise in the form of cataracts, secondary glaucoma, choroidal or exudative retinal detachment or optic atrophy.
MANAGEMENT
Topical medications alone are generally insufficient in managing scleritis. In addition to cycloplegia (scopolamine 0.25% BID/QID or atropine 1% BID) and a topical steroid, scleritis indicates a systemic anti-inflammatory agents as well. Treat moderate sectoral or diffuse anterior scleritis with oral NSAIDs (e.g., ibuprofen 600mg QID or indomethacin 25mg TID).
If the inflammation is severe or necrotizing, or if non-steroidals alone fail to suppress the inflammation, use a systemic steroid such as oral prednisone 80mg QD for two to three days, then slowly taper to 10 to 20mg daily. It may also be necessary for patients to receive a small maintenance dose for up to one month to control the condition. In rare cases, the patient may require immunosuppressive agents and should be managed by a rheumatologist.
CLINICAL PEARLS
Treated improperly, scleritis can render a great deal of damage to the affected eye.
Be sure to distinguish between this disorder and the less threatening episcleritis.
Occasionally, an atypical presentation of necrotizing scleritis without inflammation may occur; this is known as scleromalacia perforans. In this presentation, the sclera thins significantly in discrete areas, allowing for local outpouchings of the underlying choroid. There is no recognized treatment for this condition.
In all cases of scleritis, always consider the underlying cause to be systemic disease until proven otherwise. Refer patients for a comprehensive medical evaluation, including serology and radiology studies where appropriate. Specific tests may include: complete blood count (CBC) with differential, erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), HLA-B27, rheumatoid factor (RF), angiotensin-converting enzyme (ACE), fluorescent treponemal antibody absorption (FTA-ABS), lyme titer, chest X-ray and sacroiliac joint films.
Episcleritis
SIGNS AND SYMPTOMS
Episcleritis presents as a relatively asymptomatic acute onset redness in one or both eyes. Typically, you'll observe a sectoral injection of the episcleral and overlying conjunctival vessels, although the redness may be diffuse throughout these tissues. Occasionally, there may be a translucent white nodule centrally within the inflamed area (nodular episcleritis). While some patients complain of mild pain or tenderness to the affected region, particularly upon manipulation, often there is no associated discomfort. The cornea remains clear in this condition, although long-standing or recurrent episcleritis may lead to dellen formation. There is no associated anterior chamber reaction.
PATHOPHYSIOLOGY
A benign inflammatory condition of the external eye, episcleritis is seen most commonly in young adults. Women appear to be affected slightly more often than men. The disorder is idiopathic in the majority of cases, however in certain instances there may be an association with some underlying systemic disease such as rheumatoid arthritis, polyarteritis nodosa, systemic lupus erythematosus, inflammatory bowel disease, sarcoidosis, Wegener's granulomatosis, gout, herpes zoster virus or syphilis.
MANAGEMENT
Most cases of episcleritis are self-limiting, meaning that they will resolve spontaneously within two to three weeks even if the patient does not undergo treatment. However, patients who are experiencing discomfort may benefit from a regimen of topical anti-inflammatory agents and lubricants.
Typically, prednisolone acetate 1% or fluorometholone acetate applied Q3-4H will speed resolution and decrease the tenderness. The patient may use cold compresses and artificial tears liberally if discomfort persists. More severe cases, particularly nodular episcleritis, may require oral NSAIDs to quell the inflammation.
Re-examine patients weekly. For those on topical steroid therapy for more than two weeks, perform tonometry to monitor for elevation of IOP. Because of the association with systemic disorders, refer patients with extremely severe presentations or more than three recurrences for a medical evaluation.
CLINICAL PEARLS
Episcleritis is one of those conditions, like subconjunctival hemorrhage, that typically looks worse than it is. Reassure patients that they do not have "pink-eye." However, be sure to distinguish this condition from the more severe scleritis, which is far more painful and may have more serious implications.
In severe or diffuse cases in which the differential diagnosis is more difficult, blanching the conjunctiva and episclera with phenylephrine 2.5% will allow for better evaluation of the underlying sclera.
When searching for the cause of episcleritis, remember that inflammatory bowel disease, ulcerative colitis, and Crohn's disease are the most commonly associated systemic disorders.
Episcleritis presents as a relatively asymptomatic acute onset redness in one or both eyes. Typically, you'll observe a sectoral injection of the episcleral and overlying conjunctival vessels, although the redness may be diffuse throughout these tissues. Occasionally, there may be a translucent white nodule centrally within the inflamed area (nodular episcleritis). While some patients complain of mild pain or tenderness to the affected region, particularly upon manipulation, often there is no associated discomfort. The cornea remains clear in this condition, although long-standing or recurrent episcleritis may lead to dellen formation. There is no associated anterior chamber reaction.
PATHOPHYSIOLOGY
A benign inflammatory condition of the external eye, episcleritis is seen most commonly in young adults. Women appear to be affected slightly more often than men. The disorder is idiopathic in the majority of cases, however in certain instances there may be an association with some underlying systemic disease such as rheumatoid arthritis, polyarteritis nodosa, systemic lupus erythematosus, inflammatory bowel disease, sarcoidosis, Wegener's granulomatosis, gout, herpes zoster virus or syphilis.
MANAGEMENT
Most cases of episcleritis are self-limiting, meaning that they will resolve spontaneously within two to three weeks even if the patient does not undergo treatment. However, patients who are experiencing discomfort may benefit from a regimen of topical anti-inflammatory agents and lubricants.
Typically, prednisolone acetate 1% or fluorometholone acetate applied Q3-4H will speed resolution and decrease the tenderness. The patient may use cold compresses and artificial tears liberally if discomfort persists. More severe cases, particularly nodular episcleritis, may require oral NSAIDs to quell the inflammation.
Re-examine patients weekly. For those on topical steroid therapy for more than two weeks, perform tonometry to monitor for elevation of IOP. Because of the association with systemic disorders, refer patients with extremely severe presentations or more than three recurrences for a medical evaluation.
CLINICAL PEARLS
Episcleritis is one of those conditions, like subconjunctival hemorrhage, that typically looks worse than it is. Reassure patients that they do not have "pink-eye." However, be sure to distinguish this condition from the more severe scleritis, which is far more painful and may have more serious implications.
In severe or diffuse cases in which the differential diagnosis is more difficult, blanching the conjunctiva and episclera with phenylephrine 2.5% will allow for better evaluation of the underlying sclera.
When searching for the cause of episcleritis, remember that inflammatory bowel disease, ulcerative colitis, and Crohn's disease are the most commonly associated systemic disorders.
Conjunctival Laceration
SIGNS AND SYMPTOMS
Because the conjunctiva is far less innervated than the cornea, conjunctival abrasions and lacerations are less symptomatic than corneal abrasions of the same severity. Patients will present with a history of ocular trauma and complain of mild pain or a scratchy, foreign-body sensation in the affected eye. There may be some tearing and photophobia; vision is rarely impaired. The adjacent vessels will be dilated, and there will often be a subconjunctival hemorrhage. With the slit lamp, the affected region of the conjunctiva will appear torn and the edges may be retracted, revealing the underlying sclera. Fluorescein will pool in the area of the laceration under the cobalt filter. Eventually, stain will seep underneath the conjunctiva and produce a generalized "glow" to that part of the eye. Be careful to differentiate this pattern of staining from simple accumulation of fluorescein within the physiologic folds of the conjunctiva.
PATHOPHYSIOLOGY
Although the conjunctiva is normally a tough, resilient tissue, it may be lacerated in cases of ocular trauma with sharp or pointed objects such as fingernails, tree branches or the edge of a piece of paper. In these cases, the trauma itself acts as an antigen and sets off an inflammatory cascade resulting in vasodilation and edema of the involved and surrounding tissues. Rarely is there significant white cell proliferation to the point of causing an anterior chamber reaction.
MANAGEMENT
As with any case of ocular trauma, it is important to rule out global perforation. We recommend using the Seidel test, in which you apply fluorescein to the laceration and look carefully for external leakage of aqueous. Also meticulously inspect the surrounding area to look for subconjunctival foreign bodies. Once you are certain that there are no perforations or other complications, begin treatment. If the involved area of conjunctiva is small, use a broad spectrum antibiotic (Polytrim solution Q3-4H, gentamicin solution or ointment QID, or Polysporin ointment QID) and examine the patient again in three to five days. Patching is generally not necessary for smaller lesions.
If the laceration is larger, first apply topical anesthesia and use a forceps or moistened cotton-tipped applicator to manipulate any ragged areas of conjunctiva back into position. Then instill an antibiotic ointment and pressure-patch the eye for 24 hours. While most conjunctival lacerations resolve without surgical repair, significantly large (i.e., greater than 2cm) wounds may require suturing. This should only be performed by a qualified optometrist or ophthalmologist.
CLINICAL PEARLS
Conjunctival lacerations are a minor problem that typically resolve with minimal intervention, yet patients often present with great anxiety. The fact that the eye is very red and often hemorrhaging may be cause for great concern on the patient's part, even though there is little pain or other symptoms. While it's important to rule out a penetrating injury, you can safely reassure most patients that they have a simple "cut" on their eye, and that it will heal in a few days.
Because the conjunctiva is far less innervated than the cornea, conjunctival abrasions and lacerations are less symptomatic than corneal abrasions of the same severity. Patients will present with a history of ocular trauma and complain of mild pain or a scratchy, foreign-body sensation in the affected eye. There may be some tearing and photophobia; vision is rarely impaired. The adjacent vessels will be dilated, and there will often be a subconjunctival hemorrhage. With the slit lamp, the affected region of the conjunctiva will appear torn and the edges may be retracted, revealing the underlying sclera. Fluorescein will pool in the area of the laceration under the cobalt filter. Eventually, stain will seep underneath the conjunctiva and produce a generalized "glow" to that part of the eye. Be careful to differentiate this pattern of staining from simple accumulation of fluorescein within the physiologic folds of the conjunctiva.
PATHOPHYSIOLOGY
Although the conjunctiva is normally a tough, resilient tissue, it may be lacerated in cases of ocular trauma with sharp or pointed objects such as fingernails, tree branches or the edge of a piece of paper. In these cases, the trauma itself acts as an antigen and sets off an inflammatory cascade resulting in vasodilation and edema of the involved and surrounding tissues. Rarely is there significant white cell proliferation to the point of causing an anterior chamber reaction.
MANAGEMENT
As with any case of ocular trauma, it is important to rule out global perforation. We recommend using the Seidel test, in which you apply fluorescein to the laceration and look carefully for external leakage of aqueous. Also meticulously inspect the surrounding area to look for subconjunctival foreign bodies. Once you are certain that there are no perforations or other complications, begin treatment. If the involved area of conjunctiva is small, use a broad spectrum antibiotic (Polytrim solution Q3-4H, gentamicin solution or ointment QID, or Polysporin ointment QID) and examine the patient again in three to five days. Patching is generally not necessary for smaller lesions.
If the laceration is larger, first apply topical anesthesia and use a forceps or moistened cotton-tipped applicator to manipulate any ragged areas of conjunctiva back into position. Then instill an antibiotic ointment and pressure-patch the eye for 24 hours. While most conjunctival lacerations resolve without surgical repair, significantly large (i.e., greater than 2cm) wounds may require suturing. This should only be performed by a qualified optometrist or ophthalmologist.
CLINICAL PEARLS
Conjunctival lacerations are a minor problem that typically resolve with minimal intervention, yet patients often present with great anxiety. The fact that the eye is very red and often hemorrhaging may be cause for great concern on the patient's part, even though there is little pain or other symptoms. While it's important to rule out a penetrating injury, you can safely reassure most patients that they have a simple "cut" on their eye, and that it will heal in a few days.
Chlamydial & Gonococcal Conjunctivitis
SIGNS AND SYMPTOMS
Chlamydial (inclusion) conjunctivitis typically affects sexually active teens and young adults and is the most frequent infectious cause of neonatal conjunctivitis in the U.S. The Centers for Disease Control (CDC) recognizes chlamydia as one of the major sexually transmitted pathogens, estimating approximately three million new cases per year. Women seem to be more susceptible than men. The incidence of infection seems to be directly related to sexual activity and geography, with urban populations having higher incidences. The incidence in pregnant women overall is 4 to 10 percent.
Diagnosis of inclusion conjunctivitis is often difficult. Many times there are little, if any, symptoms. Infants whose mothers have untreated chlamydial infection have a 30 to 40 percent chance of developing neonatal chlamydial conjunctivitis. Systemic signs and symptoms may include a history of vaginitis, pelvic inflammatory disease or urethritis.
Ocular signs and symptoms include the chief complaint that an eye infection has persisted for over three weeks despite treatment with topical antibiotics. Conjunctival injection, superficial punctate keratitis, superior corneal pannus, peripheral subepithelial infiltrates, iritis and follicles (most dense in the inferior cul-de-sac) may all be present. Mucopurulent, stringy or mucus discharge is common. A palpable preauricular node is almost always present.
Gonococcal conjunctivitis, sometimes referred to as hyperacute conjunctivitis, is also a sexually transmitted ocular disease. While sexual contact is the customary route of transmission, even casual interaction with infected individuals has been reported as a cause. Newborn infants may acquire the infection by passing through an infected birth canal. Systemically, gonococcal infections are associated with infection of the urethra, cervix and rectum. Symptoms vary from nothing to discharge and irritation.
This unusually contagious ocular disease typically presents as a hyperacute red eye of less than four weeks duration with foreign body sensation; the eye may be “glued” shut with severe purulent discharge. The conjunctivitis has an incubation period of two to seven days. Conjunctival papillae, superficial punctate keratitis and marked chemosis are almost always present. Subconjunctival hemorrhage (hemorrhagic conjunctivitis), pseudomembrane or true membrane formation and preauricular lymph nodes are usually present. In chronic, recalcitrant or severe cases, peripheral subepithelial corneal infiltrates may occur, leading to marginal ulceration with anterior uveitis.
PATHOPHYSIOLOGY
Chlamydia trachomatis is an intracellular parasite that contains its own DNA and RNA. The sub-group A causes chlamydial infections, the serotypes A, B, Ba and C cause trachoma, and serotypes D through K produce adult inclusion conjunctivitis. The mode of ocular transmission may be hand contact from a site of genital infection to the eye, laboratory accidents, a mother infecting the newborn, shared cosmetics and occasionally an improperly chlorinated hot tub.
Diagnostic testing for chlamydia is expensive and difficult to interpret. The preferred method of identification is to culture the organism. Conjunctival scrapings for Giemsa staining will show intracytoplasmic inclusion bodies in epithelial cells, polymorphonuclear leukocytes and lymphocytes.
The infectious organism in gonococcal conjunctivitis is Neisseria gonorrhoeae, a gram-negative, intracellular diplococcus capable of invading an intact mucosal membrane. Transmission is generally by direct or indirect sexual contact or contact with an infected individual. N. gonorrhoeae’s ability to penetrate an intact corneal epithelium makes the risk of corneal infection and ulceration high.
MANAGEMENT
In treating chlamydial conjunctivitis, many doctors consider oral tetracycline 250 to 500mg q.i.d. for three weeks the treatment of first choice. But since tetracycline must be administered one hour before or after meals to avoid gastrointestinal side effects and interference of dairy products with its efficacy, other oral medications may be more appropriate. Amoxacillin and erythromycin 250 to 500mg q.i.d. for three weeks or doxycycline 100mg b.i.d. for one week are acceptable alternatives.
Currently, the drug of choice is azithromycin (Zithromax). Taken as a 1 gram dose, by mouth, one time, it has been documented as being as effective for the treatment of genital chlamydial infection as doxycycline. Topical therapy is adjunctive and includes erythromicin, tetracycline or sulfacetamide t.i.d. for three weeks as well.
Patients with gonococcal conjunctivitis require immediate conjunctival scrapings for culture and sensitivity testing. Medical management of gonococcal infection begins with an intramuscular loading dose of ceftriaxone 1g. Ideally, the patient should be hospitalized and given one gram of ceftriaxone intravenously within 12 to 24 hours. Following discharge, resume treatment with either erythromicin 250 to 500mg p.o. q.i.d., tetracycline 250 to 500mg p.o. q.i.d. or doxycycline 100mg p.o. b.i.d.
Begin ocular management with saline lavage to clear the mucopurulent debris from the lids and conjunctiva. A topical fluoroquinolone (ofloxacin or ciprofloxacin) is appropriate if corneal infection occurs. However, because gonococcal conjunctivitis does not respond to topical antibiotics, topical therapy is usually not indicated.
CLINICAL PEARLS
Chlamydial (inclusion) conjunctivitis typically affects sexually active teens and young adults and is the most frequent infectious cause of neonatal conjunctivitis in the U.S. The Centers for Disease Control (CDC) recognizes chlamydia as one of the major sexually transmitted pathogens, estimating approximately three million new cases per year. Women seem to be more susceptible than men. The incidence of infection seems to be directly related to sexual activity and geography, with urban populations having higher incidences. The incidence in pregnant women overall is 4 to 10 percent.
Diagnosis of inclusion conjunctivitis is often difficult. Many times there are little, if any, symptoms. Infants whose mothers have untreated chlamydial infection have a 30 to 40 percent chance of developing neonatal chlamydial conjunctivitis. Systemic signs and symptoms may include a history of vaginitis, pelvic inflammatory disease or urethritis.
Ocular signs and symptoms include the chief complaint that an eye infection has persisted for over three weeks despite treatment with topical antibiotics. Conjunctival injection, superficial punctate keratitis, superior corneal pannus, peripheral subepithelial infiltrates, iritis and follicles (most dense in the inferior cul-de-sac) may all be present. Mucopurulent, stringy or mucus discharge is common. A palpable preauricular node is almost always present.
Gonococcal conjunctivitis, sometimes referred to as hyperacute conjunctivitis, is also a sexually transmitted ocular disease. While sexual contact is the customary route of transmission, even casual interaction with infected individuals has been reported as a cause. Newborn infants may acquire the infection by passing through an infected birth canal. Systemically, gonococcal infections are associated with infection of the urethra, cervix and rectum. Symptoms vary from nothing to discharge and irritation.
This unusually contagious ocular disease typically presents as a hyperacute red eye of less than four weeks duration with foreign body sensation; the eye may be “glued” shut with severe purulent discharge. The conjunctivitis has an incubation period of two to seven days. Conjunctival papillae, superficial punctate keratitis and marked chemosis are almost always present. Subconjunctival hemorrhage (hemorrhagic conjunctivitis), pseudomembrane or true membrane formation and preauricular lymph nodes are usually present. In chronic, recalcitrant or severe cases, peripheral subepithelial corneal infiltrates may occur, leading to marginal ulceration with anterior uveitis.
PATHOPHYSIOLOGY
Chlamydia trachomatis is an intracellular parasite that contains its own DNA and RNA. The sub-group A causes chlamydial infections, the serotypes A, B, Ba and C cause trachoma, and serotypes D through K produce adult inclusion conjunctivitis. The mode of ocular transmission may be hand contact from a site of genital infection to the eye, laboratory accidents, a mother infecting the newborn, shared cosmetics and occasionally an improperly chlorinated hot tub.
Diagnostic testing for chlamydia is expensive and difficult to interpret. The preferred method of identification is to culture the organism. Conjunctival scrapings for Giemsa staining will show intracytoplasmic inclusion bodies in epithelial cells, polymorphonuclear leukocytes and lymphocytes.
The infectious organism in gonococcal conjunctivitis is Neisseria gonorrhoeae, a gram-negative, intracellular diplococcus capable of invading an intact mucosal membrane. Transmission is generally by direct or indirect sexual contact or contact with an infected individual. N. gonorrhoeae’s ability to penetrate an intact corneal epithelium makes the risk of corneal infection and ulceration high.
MANAGEMENT
In treating chlamydial conjunctivitis, many doctors consider oral tetracycline 250 to 500mg q.i.d. for three weeks the treatment of first choice. But since tetracycline must be administered one hour before or after meals to avoid gastrointestinal side effects and interference of dairy products with its efficacy, other oral medications may be more appropriate. Amoxacillin and erythromycin 250 to 500mg q.i.d. for three weeks or doxycycline 100mg b.i.d. for one week are acceptable alternatives.
Currently, the drug of choice is azithromycin (Zithromax). Taken as a 1 gram dose, by mouth, one time, it has been documented as being as effective for the treatment of genital chlamydial infection as doxycycline. Topical therapy is adjunctive and includes erythromicin, tetracycline or sulfacetamide t.i.d. for three weeks as well.
Patients with gonococcal conjunctivitis require immediate conjunctival scrapings for culture and sensitivity testing. Medical management of gonococcal infection begins with an intramuscular loading dose of ceftriaxone 1g. Ideally, the patient should be hospitalized and given one gram of ceftriaxone intravenously within 12 to 24 hours. Following discharge, resume treatment with either erythromicin 250 to 500mg p.o. q.i.d., tetracycline 250 to 500mg p.o. q.i.d. or doxycycline 100mg p.o. b.i.d.
Begin ocular management with saline lavage to clear the mucopurulent debris from the lids and conjunctiva. A topical fluoroquinolone (ofloxacin or ciprofloxacin) is appropriate if corneal infection occurs. However, because gonococcal conjunctivitis does not respond to topical antibiotics, topical therapy is usually not indicated.
CLINICAL PEARLS
Bacterial Conjunctivitis
SIGNS AND SYMPTOMS
Patients with bacterial conjunctival infections present with injection of the bulbar conjunctiva, episcleral vessels and perhaps papillae of the palpebral conjunctiva. The infection often starts in one eye, then soon spreads to the other. There will be thick mucopurulent discharge, and patients usually say that their eyelids and eyelashes are matted shut upon awakening. There may be mild photophobia and discomfort, but usually no pain. Visual function is normal in most cases.
PATHOPHYSIOLOGY
The eye has a battery of defenses to prevent bacterial invasion. These include bacteriostatic lysozymes and immunoglobulins in the tear film, the shearing force of the blink, the immune system in general, and non-pathogenic bacteria that colonize the eye and compete against external organisms that try to enter. When any of these defense mechanisms break down, pathogenic bacterial infection is possible.
Invading bacteria, and the exotoxins they produce, are considered foreign antigens. This induces an antigen-antibody immune reaction and subsequently causes inflammation. In a normal, healthy person the eye will fight to return to homeostasis, and the bacteria will eventually be eradicated. However, an extra heavy load of external organisms can be too difficult to fight off, causing a conjunctival infection and setting the eye up for potential corneal infection.
The most commonly encountered organisms are Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa. In cases of hyperacute bacterial conjunctivitis, the patient will present with similar signs and symptoms, albeit much more severe. The most common infectious organisms in hyperacute conjunctivitis are Neisseria gonorrhoeae and Corynebacterium diptheroides. There is more danger in hyperacute bacterial conjunctivitis as these organisms can penetrate an intact cornea.
MANAGEMENT
Ordering cultures and sensitivity tests is ideal for diagnosis but usually impractical and expensive. Most clinicians immediately begin treatment with a broad spectrum antibiotic and reserve culturing for hyperacute conditions or those that fail to respond to the initial therapy.
There are many antibacterial options. Excellent initial broad spectrum antibiotics include Polytrim (polymixin B sulfate and trimethoprim sulfate), gentamicin 0.3%, and tobramycin 0.3%. These will give good coverage of gram-positive and gram-negative organisms, though the aminoglycosides (gentamicin and tobramycin) have weak activity against Staphylococcal species; there are also resistant strains of Pseudomonas. Fluoroquinolones such as Ciloxan, Ocuflox and Chibroxin are also excellent options. Therapy should be aggressive, with administration from QID to Q1H for the first few days.
Although antibiotics will eradicate the bacteria, they will do nothing to suppress the concurrent inflammation. If there is no significant corneal disruption, prescribe a steroid such as Pred Forte, Vexol or Flarex along with your antibiotic of choice, or a steroid-antibiotic combination such as Maxitrol (neomycin, polymyxin B, dexamethasone 0.1%), Pred-G (gentamicin 0.3%, prednisolone acetate 0.1%), or Tobradex (tobramycin 0.3%, dexamethasone 0.1%).
CLINICAL PEARLS
Like patients with bacterial conjunctivitis, those suffering from viral and allergic conjunctivitis will often report that their lids are matted shut in the morning with mucopurulent material. However, these patients actually have crusting of the lashes due to drying of tears and serous secretions, not the wet, sticky, mucopurulent matting characteristic of bacterial conjunctivitis. Too often, clinicians will consider the crusting of the lashes to be the same as the mucopurulent matting and misdiagnose the condition.
Remember, due to the excellent defense systems of the eye, acute bacterial conjunctivitis is uncommon.
Patients with bacterial conjunctival infections present with injection of the bulbar conjunctiva, episcleral vessels and perhaps papillae of the palpebral conjunctiva. The infection often starts in one eye, then soon spreads to the other. There will be thick mucopurulent discharge, and patients usually say that their eyelids and eyelashes are matted shut upon awakening. There may be mild photophobia and discomfort, but usually no pain. Visual function is normal in most cases.
PATHOPHYSIOLOGY
The eye has a battery of defenses to prevent bacterial invasion. These include bacteriostatic lysozymes and immunoglobulins in the tear film, the shearing force of the blink, the immune system in general, and non-pathogenic bacteria that colonize the eye and compete against external organisms that try to enter. When any of these defense mechanisms break down, pathogenic bacterial infection is possible.
Invading bacteria, and the exotoxins they produce, are considered foreign antigens. This induces an antigen-antibody immune reaction and subsequently causes inflammation. In a normal, healthy person the eye will fight to return to homeostasis, and the bacteria will eventually be eradicated. However, an extra heavy load of external organisms can be too difficult to fight off, causing a conjunctival infection and setting the eye up for potential corneal infection.
The most commonly encountered organisms are Staphylococcus aureus, Haemophilus influenzae, Streptococcus pneumoniae and Pseudomonas aeruginosa. In cases of hyperacute bacterial conjunctivitis, the patient will present with similar signs and symptoms, albeit much more severe. The most common infectious organisms in hyperacute conjunctivitis are Neisseria gonorrhoeae and Corynebacterium diptheroides. There is more danger in hyperacute bacterial conjunctivitis as these organisms can penetrate an intact cornea.
MANAGEMENT
Ordering cultures and sensitivity tests is ideal for diagnosis but usually impractical and expensive. Most clinicians immediately begin treatment with a broad spectrum antibiotic and reserve culturing for hyperacute conditions or those that fail to respond to the initial therapy.
There are many antibacterial options. Excellent initial broad spectrum antibiotics include Polytrim (polymixin B sulfate and trimethoprim sulfate), gentamicin 0.3%, and tobramycin 0.3%. These will give good coverage of gram-positive and gram-negative organisms, though the aminoglycosides (gentamicin and tobramycin) have weak activity against Staphylococcal species; there are also resistant strains of Pseudomonas. Fluoroquinolones such as Ciloxan, Ocuflox and Chibroxin are also excellent options. Therapy should be aggressive, with administration from QID to Q1H for the first few days.
Although antibiotics will eradicate the bacteria, they will do nothing to suppress the concurrent inflammation. If there is no significant corneal disruption, prescribe a steroid such as Pred Forte, Vexol or Flarex along with your antibiotic of choice, or a steroid-antibiotic combination such as Maxitrol (neomycin, polymyxin B, dexamethasone 0.1%), Pred-G (gentamicin 0.3%, prednisolone acetate 0.1%), or Tobradex (tobramycin 0.3%, dexamethasone 0.1%).
CLINICAL PEARLS
Like patients with bacterial conjunctivitis, those suffering from viral and allergic conjunctivitis will often report that their lids are matted shut in the morning with mucopurulent material. However, these patients actually have crusting of the lashes due to drying of tears and serous secretions, not the wet, sticky, mucopurulent matting characteristic of bacterial conjunctivitis. Too often, clinicians will consider the crusting of the lashes to be the same as the mucopurulent matting and misdiagnose the condition.
Remember, due to the excellent defense systems of the eye, acute bacterial conjunctivitis is uncommon.
Squamous Cell Carcinoma
Signs and Symptoms
Squamous cell carcinoma is the second most common malignant eyelid neoplasm in the United States, after basal cell carcinoma.
It is most often encountered in elderly, fair-skinned individuals who have a history of chronic sun exposure. Patients presenting with this lesion may demonstrate a roughened scaly patch of tissue on or near the lid margin or in the canthal region. The area is typically red, elevated and nodular, with crusted and/or bloody margins. Often, patients describe this lesion as “a non-healing scab.” According to one study, the most common presentation involves nodular ulceration as the disease progresses, resulting in hemorrhagic or purulent discharge.
Squamous cell carcinoma in its early stages is easily confused with a multitude of other eyelid lesions, both malignant and benign. Some of these lesions include basal cell carcinoma, sebaceous gland carcinoma, follicular keratosis, actinic keratosis, seborrheic keratosis, and keratoacanthoma.
Rarely are patients with squamous cell carcinoma symptomatic, displaying only mild irritation in most cases. Acuity is not affected unless the lesion is so large as to obscure the visual axis.
Pathophysiology
Squamous cell carcinoma is a potentially invasive tumor derived from surface epithelium. In the early stages, the normal epithelial cells are replaced by atypical squamous cells throughout the epidermis, resulting in a loss of normal maturation. This stage is sometimes referred to as squamous cell carcinoma in situ. After the dysplastic squamous cells encroach beyond the borders of the basement membrane, the lesion is referred to as invasive squamous cell carcinoma.
While no single causative agent for the development of squamous cell carcinoma has been identified, it is clear that ultraviolet radiation is a substantial risk factor and demonstrates a distinct association with this disease. This is supported by the fact that the majority of squamous cell tumors arise on the lower lid margin and medial canthus, the two periocular areas most susceptible to sunlight exposure. Increasing age and northern European descent are two other commonly associated factors in patients with squamous cell carcinoma.
Management
The management of squamous cell carcinoma is virtually identical to that of basal cell carcinoma of the lid. These lesions may be treated with surgical excision, radiation therapy, chemotherapy, or cryotherapy. The preferred course for most cases is surgery, with broad margins to ensure complete removal. Frozen tissue sections of the tumor borders are evaluated intraoperatively to further assure that the lesion is excised completely (Mohs micrographic technique). This method offers the greatest success with the least incidence of recurrence. Local radiation and/or systemic chemotherapy may be used in managing squamous cell carcinoma when surgery is intolerable or refused by the patient. Both of these modalities carry significant side effects, and neither is as efficacious as surgical intervention. Cryotherapy has been used somewhat effectively for smaller tumors, but does not ensure complete tumor eradication, and therefore results in a high recurrence.
Clinical Pearls
Squamous cell carcinoma represents approximately
5 percent of all eyelid malignancies. While this particular neoplasm does possess the ability to invade local tissues and metastasize to other organ systems, it is not a particularly aggressive tumor. Its rate of development is quite slow, and metastasis is exceedingly rare. Still, the potential for damage exists in cases where diagnosis and treatment are delayed.
Early biopsy is often the key to diagnosis. Suspicious lid lesions, which demonstrate irregular growth, changes in color or appearance, or discharge of a purulent or bloody nature should be biopsied to rule out cancerous entities. Confirmed malignancies should be referred promptly for treatment by an oculoplastics specialist or, where possible, an ocular oncologist.
Squamous cell carcinoma is the second most common malignant eyelid neoplasm in the United States, after basal cell carcinoma.
It is most often encountered in elderly, fair-skinned individuals who have a history of chronic sun exposure. Patients presenting with this lesion may demonstrate a roughened scaly patch of tissue on or near the lid margin or in the canthal region. The area is typically red, elevated and nodular, with crusted and/or bloody margins. Often, patients describe this lesion as “a non-healing scab.” According to one study, the most common presentation involves nodular ulceration as the disease progresses, resulting in hemorrhagic or purulent discharge.
Squamous cell carcinoma in its early stages is easily confused with a multitude of other eyelid lesions, both malignant and benign. Some of these lesions include basal cell carcinoma, sebaceous gland carcinoma, follicular keratosis, actinic keratosis, seborrheic keratosis, and keratoacanthoma.
Rarely are patients with squamous cell carcinoma symptomatic, displaying only mild irritation in most cases. Acuity is not affected unless the lesion is so large as to obscure the visual axis.
Pathophysiology
Squamous cell carcinoma is a potentially invasive tumor derived from surface epithelium. In the early stages, the normal epithelial cells are replaced by atypical squamous cells throughout the epidermis, resulting in a loss of normal maturation. This stage is sometimes referred to as squamous cell carcinoma in situ. After the dysplastic squamous cells encroach beyond the borders of the basement membrane, the lesion is referred to as invasive squamous cell carcinoma.
While no single causative agent for the development of squamous cell carcinoma has been identified, it is clear that ultraviolet radiation is a substantial risk factor and demonstrates a distinct association with this disease. This is supported by the fact that the majority of squamous cell tumors arise on the lower lid margin and medial canthus, the two periocular areas most susceptible to sunlight exposure. Increasing age and northern European descent are two other commonly associated factors in patients with squamous cell carcinoma.
Management
The management of squamous cell carcinoma is virtually identical to that of basal cell carcinoma of the lid. These lesions may be treated with surgical excision, radiation therapy, chemotherapy, or cryotherapy. The preferred course for most cases is surgery, with broad margins to ensure complete removal. Frozen tissue sections of the tumor borders are evaluated intraoperatively to further assure that the lesion is excised completely (Mohs micrographic technique). This method offers the greatest success with the least incidence of recurrence. Local radiation and/or systemic chemotherapy may be used in managing squamous cell carcinoma when surgery is intolerable or refused by the patient. Both of these modalities carry significant side effects, and neither is as efficacious as surgical intervention. Cryotherapy has been used somewhat effectively for smaller tumors, but does not ensure complete tumor eradication, and therefore results in a high recurrence.
Clinical Pearls
Squamous cell carcinoma represents approximately
5 percent of all eyelid malignancies. While this particular neoplasm does possess the ability to invade local tissues and metastasize to other organ systems, it is not a particularly aggressive tumor. Its rate of development is quite slow, and metastasis is exceedingly rare. Still, the potential for damage exists in cases where diagnosis and treatment are delayed.
Early biopsy is often the key to diagnosis. Suspicious lid lesions, which demonstrate irregular growth, changes in color or appearance, or discharge of a purulent or bloody nature should be biopsied to rule out cancerous entities. Confirmed malignancies should be referred promptly for treatment by an oculoplastics specialist or, where possible, an ocular oncologist.
Sunday, December 19, 2010
Viral Conjunctivitis (Pharyngoconjunctival Fever & Epidemic Keratoconjunctivitis)
SIGNS AND SYMPTOMS
Most viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe, disabling visual difficulties. The two most common self-limiting forms of viral conjunctivitis are epidemic keratoconjunctivitis and pharyngoconjunctival fever.
Pharyngoconjunc-tival fever (PCF) is characterized by fever, sore throat and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and occasionally 4 or 7. Corneal infiltrates are rare. The disorder varies in severity but usually persists for four days to two weeks. While the virus is shed from the conjunctiva within 14 days, it remains in fecal matter for 30 days.
Epidemic Keratoconjunctivitis (EKC) often presents as a bilateral, inferior, palpebral, follicular conjunctivitis, with epithelial and stromal keratitis. Subepithelial corneal infiltrates are much more common in EKC than in PCF and are typically concentrated in the central cornea. EKC is regularly caused by adenovirus types 8 and 19.
The key clinical signs of both conditions include: conjunctival injection, tearing, serous discharge, edematous eyelids, pinpoint subconjunctival hemorrhages, pseudomembrane formation and palpable preauricular lymph nodes. In severe cases, conjunctival desiccation causes scarring and symblepharon formation (adherence of the bulbar and palpebral conjunctivas).
Both conditions are highly contagious. Patients will usually report recent contact with someone who had either red eyes or an upper respiratory infection. Both forms tend to start in one eye, then spread to the other eye within a few days. In rare cases, the focal subconjunctival hemorrhages can evolve into acute hemorrhagic conjunctivitis.
PATHOPHYSIOLOGY
Viral conjunctival infections are thought to be caused by airborne respiratory droplets or direct transfer from one’s fingers to the conjunctival surface of the eyelids. After an incubation period of five to 12 days, the disease enters the acute phase, causing watery discharge, conjunctival hyperemia and follicle formation. Lymphoid follicles are elevated, with avascular lesions ranging from 0.2 to 2mm in size. They have lymphoid germinal centers that have responded to an infectious agent.
Adenovirus type 8 can proliferate in the corneal epithelial tissues, producing the characteristic keratitis and subepithelial infiltrates. This, along with the immune response to viral antigens, causes lymphocytes to collect in the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These are made up of fibrin and leukocytes, and in prolonged cases, of fibroblast and collagen deposits. “Pseudomembranes” are much easier to remove than “true” membranes.
MANAGEMENT
Because EKC and PCF are contagious and self-limiting, the primary treatment once again is patient education. Instruct patients to stay home from work or school until there is absolutely no discharge. Also instruct them not to share utensils, glasses, linens or wash cloths with others.
Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g., naphazoline) and steroids (Vexol, Flarex, Pred Forte) two to four times daily. If a membrane is present, peel it off with a wet, cotton-tipped applicator or forceps. After removal, prescribe a topical antibiotic-steroid combination such as Tobradex or Maxitrol q.i.d. Anti-viral drugs such as Viroptic are ineffective against adenovirus.
Recently, there has been a breakthrough in the management of adenoviral keratoconjunctivitis. Cidofovir (Vistide), an anti-viral drug used intravenously to treat cytomegalovirus retinitis, appears to be effective in adenoviral keratoconjunctivitis. The topical form creates a faulty viral DNA structure. Twice daily instillation is recommended. This topical anti-viral is also possibly effective against herpes simplex and zoster, and Epstein-Barr virus.
CLINICAL PEARLS
Keep your equipment, instruments and chair area meticulously clean to avoid contaminating your patients and staff.
Most practitioners reserve topical steroidal therapy for severe cases (if the infection is on the visual axis and affecting acuity, for example), or recalcitrant cases. EKC infiltrates resolve without scarring the cornea.
Tell patients to expect the symptoms to get worse for about seven to 10 days before getting better, and that the infection won’t completely go away for three to six weeks. Remember to always taper steroids slowly as the condition recedes.
Most viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe, disabling visual difficulties. The two most common self-limiting forms of viral conjunctivitis are epidemic keratoconjunctivitis and pharyngoconjunctival fever.
Pharyngoconjunc-tival fever (PCF) is characterized by fever, sore throat and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and occasionally 4 or 7. Corneal infiltrates are rare. The disorder varies in severity but usually persists for four days to two weeks. While the virus is shed from the conjunctiva within 14 days, it remains in fecal matter for 30 days.
Epidemic Keratoconjunctivitis (EKC) often presents as a bilateral, inferior, palpebral, follicular conjunctivitis, with epithelial and stromal keratitis. Subepithelial corneal infiltrates are much more common in EKC than in PCF and are typically concentrated in the central cornea. EKC is regularly caused by adenovirus types 8 and 19.
The key clinical signs of both conditions include: conjunctival injection, tearing, serous discharge, edematous eyelids, pinpoint subconjunctival hemorrhages, pseudomembrane formation and palpable preauricular lymph nodes. In severe cases, conjunctival desiccation causes scarring and symblepharon formation (adherence of the bulbar and palpebral conjunctivas).
Both conditions are highly contagious. Patients will usually report recent contact with someone who had either red eyes or an upper respiratory infection. Both forms tend to start in one eye, then spread to the other eye within a few days. In rare cases, the focal subconjunctival hemorrhages can evolve into acute hemorrhagic conjunctivitis.
PATHOPHYSIOLOGY
Viral conjunctival infections are thought to be caused by airborne respiratory droplets or direct transfer from one’s fingers to the conjunctival surface of the eyelids. After an incubation period of five to 12 days, the disease enters the acute phase, causing watery discharge, conjunctival hyperemia and follicle formation. Lymphoid follicles are elevated, with avascular lesions ranging from 0.2 to 2mm in size. They have lymphoid germinal centers that have responded to an infectious agent.
Adenovirus type 8 can proliferate in the corneal epithelial tissues, producing the characteristic keratitis and subepithelial infiltrates. This, along with the immune response to viral antigens, causes lymphocytes to collect in the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These are made up of fibrin and leukocytes, and in prolonged cases, of fibroblast and collagen deposits. “Pseudomembranes” are much easier to remove than “true” membranes.
MANAGEMENT
Because EKC and PCF are contagious and self-limiting, the primary treatment once again is patient education. Instruct patients to stay home from work or school until there is absolutely no discharge. Also instruct them not to share utensils, glasses, linens or wash cloths with others.
Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g., naphazoline) and steroids (Vexol, Flarex, Pred Forte) two to four times daily. If a membrane is present, peel it off with a wet, cotton-tipped applicator or forceps. After removal, prescribe a topical antibiotic-steroid combination such as Tobradex or Maxitrol q.i.d. Anti-viral drugs such as Viroptic are ineffective against adenovirus.
Recently, there has been a breakthrough in the management of adenoviral keratoconjunctivitis. Cidofovir (Vistide), an anti-viral drug used intravenously to treat cytomegalovirus retinitis, appears to be effective in adenoviral keratoconjunctivitis. The topical form creates a faulty viral DNA structure. Twice daily instillation is recommended. This topical anti-viral is also possibly effective against herpes simplex and zoster, and Epstein-Barr virus.
CLINICAL PEARLS
Keep your equipment, instruments and chair area meticulously clean to avoid contaminating your patients and staff.
Most practitioners reserve topical steroidal therapy for severe cases (if the infection is on the visual axis and affecting acuity, for example), or recalcitrant cases. EKC infiltrates resolve without scarring the cornea.
Tell patients to expect the symptoms to get worse for about seven to 10 days before getting better, and that the infection won’t completely go away for three to six weeks. Remember to always taper steroids slowly as the condition recedes.
Allergic Conjunctivitis &Vernal Keratoconjunctivitis (VKC)
SIGNS AND SYMPTOMS
Itching and conjunctival injection are the two hallmarks of an allergic reaction. Also definitive is a lack of palpable preauricular lymph nodes, since palpable preauricular nodes signify viral infection. The eyelids may be swollen and red, and you may also see papillae of the palpebral conjunctiva. In most cases, patients will report a history of seasonal or other allergies.
Seasonal allergies typically produce a thin, watery discharge and do not involve the cornea. If the patient exhibits thick, ropy discharge with severe itching and corneal involvement, it is most likely VKC rather than a seasonal allergy. VKC’s prevalence is higher in the warmer climates. Onset is typically between the ages of three and 25 years. Males are typically more affected than females.
The important clinical signs of VKC include large conjunctival papillae on the back of the superior tarsus, Horner-Trantas dots (gelatinous, white clumps of degenerated eosinophils at the superior limbus), areas of superficial punctate keratitis (SPK) and, in severe cases, well demarcated, sterile, superiorly located corneal shield ulcers.
PATHOPHYSIOLOGY
An allergic response is an unwarranted over-reaction of the body’s immune system to foreign substances known as allergens, which the body wrongly perceives as a potential threat. The response can be innate or acquired. The presence of an allergen on the conjunctiva initiates two simultaneous immune responses, one caused by the release of so-called “pre-formed” inflammatory mediators such as histamine from mast cells, and the other by the production of arachidonic acid and its conversion into so-called “newly-formed” mediators such as prostaglandins (see “Tracing the Complex Path of Allergic Reactions,” on next page). Pre-formed mediators are released immediately upon exposure; newly-formed mediators are delayed roughly eight to 24 hours.
In mast cell degranulation, the allergen attracts and binds to an antibody known as immunoglobulin E (abbreviated as “IgE”), then adheres to mast cells and causes them to degranulate, like a key opening a lock. This discharges the pre-formed mediators. Their effects can be either direct, indirect or a combination of the two.
Two important mediators released from mast cells, histamine and bradykinin, immediately begin to stimulate nerve endings called nociceptors, creating the sensation of itching. Both also increase vascular permeability and vasodilation; this causes the clinical signs of redness and conjunctival injection.
Meanwhile, other mediators released from mast cells send out chemical signals that attract both red and white blood cells to the area. Once these cells arrive, they easily reach the conjunctival surface by moving through the dilated and highly permeable capillaries.
The body’s other defense mechanism, referred to as the arachidonic acid cascade, produces three newly-formed inflammatory mediators—prostaglandins, thromboxanes and leukotrienes—which are collectively known as eicosanoids.
Virtually all cells contain a phospholipid layer within their cell walls. Any disruption or threat signals the cell to convert phospholipids into arachidonic acid. When arachidonic acid interacts with two enzymes known as cyclooxygenase and lipoxygenase, it is metabolized into eicosanoids. An allergen’s presence initiates the arachidonic acid cascade both within conjunctival epithelial cells and also within mast cells as they degranulate.
Much like histamine and bradykinin, prostaglandins directly stimulate nerve endings to produce sensations of itching and pain, and also increase vascular permeability and vasodilation. Leukotrienes primarily attract macrophages (white blood cells).
MANAGEMENT
Management of both allergic conjunctivitis and VKC is primarily aimed at alleviating symptoms. The most effective but least practical treatment is to prevent exposure to the allergen. Since this is not usually possible, instruct patients to frequently use cold compresses, artificial tears and ointments to soothe, lubricate and wash away the allergens. Also recommend that patients use a topical decongestant such as naphazoline or phenylephrine as needed. These drugs cause vasoconstriction, retarding the release of the chemical mediators into the tissues from the blood stream. This reduces hyperemia, chemosis and other symptoms.
Mast cell stabilizers such as Alomide and Crolom help prevent the onset of allergic reactions by blocking the adherence of the IgE-allergen compound to the mast cell. Treat patients with a history of recurrent seasonal allergies using a mast cell stabilizer q.i.d. for four weeks in advance of allergy season. Patanol (olopatadine 0.1%) combines mast cell stabilization with an antihistamine to offer therapy that is for both acute and chronic symptoms. The effects last eight hours, allowing for b.i.d. rather than q.i.d. dosing.
In moderate to severe cases, recommend one or more of the following, used from two to four times per day as needed: a topical medication such as Patanol or Livostin, oral antihistamines such as Benadryl, or a topical non-steroidal anti-inflammatory drug (Acular, Voltaren or Profenal). In extremely symptomatic cases, use a topical steroid such as Vexol, Flarex or Alrex q.i.d.
Only prostaglandins and thromboxanes are produced when cyclooxygenase interacts with arachidonic acid. Leukotrienes, by contrast, are produced from the break-down of arachido
Itching and conjunctival injection are the two hallmarks of an allergic reaction. Also definitive is a lack of palpable preauricular lymph nodes, since palpable preauricular nodes signify viral infection. The eyelids may be swollen and red, and you may also see papillae of the palpebral conjunctiva. In most cases, patients will report a history of seasonal or other allergies.
Seasonal allergies typically produce a thin, watery discharge and do not involve the cornea. If the patient exhibits thick, ropy discharge with severe itching and corneal involvement, it is most likely VKC rather than a seasonal allergy. VKC’s prevalence is higher in the warmer climates. Onset is typically between the ages of three and 25 years. Males are typically more affected than females.
The important clinical signs of VKC include large conjunctival papillae on the back of the superior tarsus, Horner-Trantas dots (gelatinous, white clumps of degenerated eosinophils at the superior limbus), areas of superficial punctate keratitis (SPK) and, in severe cases, well demarcated, sterile, superiorly located corneal shield ulcers.
PATHOPHYSIOLOGY
An allergic response is an unwarranted over-reaction of the body’s immune system to foreign substances known as allergens, which the body wrongly perceives as a potential threat. The response can be innate or acquired. The presence of an allergen on the conjunctiva initiates two simultaneous immune responses, one caused by the release of so-called “pre-formed” inflammatory mediators such as histamine from mast cells, and the other by the production of arachidonic acid and its conversion into so-called “newly-formed” mediators such as prostaglandins (see “Tracing the Complex Path of Allergic Reactions,” on next page). Pre-formed mediators are released immediately upon exposure; newly-formed mediators are delayed roughly eight to 24 hours.
In mast cell degranulation, the allergen attracts and binds to an antibody known as immunoglobulin E (abbreviated as “IgE”), then adheres to mast cells and causes them to degranulate, like a key opening a lock. This discharges the pre-formed mediators. Their effects can be either direct, indirect or a combination of the two.
Two important mediators released from mast cells, histamine and bradykinin, immediately begin to stimulate nerve endings called nociceptors, creating the sensation of itching. Both also increase vascular permeability and vasodilation; this causes the clinical signs of redness and conjunctival injection.
Meanwhile, other mediators released from mast cells send out chemical signals that attract both red and white blood cells to the area. Once these cells arrive, they easily reach the conjunctival surface by moving through the dilated and highly permeable capillaries.
The body’s other defense mechanism, referred to as the arachidonic acid cascade, produces three newly-formed inflammatory mediators—prostaglandins, thromboxanes and leukotrienes—which are collectively known as eicosanoids.
Virtually all cells contain a phospholipid layer within their cell walls. Any disruption or threat signals the cell to convert phospholipids into arachidonic acid. When arachidonic acid interacts with two enzymes known as cyclooxygenase and lipoxygenase, it is metabolized into eicosanoids. An allergen’s presence initiates the arachidonic acid cascade both within conjunctival epithelial cells and also within mast cells as they degranulate.
Much like histamine and bradykinin, prostaglandins directly stimulate nerve endings to produce sensations of itching and pain, and also increase vascular permeability and vasodilation. Leukotrienes primarily attract macrophages (white blood cells).
MANAGEMENT
Management of both allergic conjunctivitis and VKC is primarily aimed at alleviating symptoms. The most effective but least practical treatment is to prevent exposure to the allergen. Since this is not usually possible, instruct patients to frequently use cold compresses, artificial tears and ointments to soothe, lubricate and wash away the allergens. Also recommend that patients use a topical decongestant such as naphazoline or phenylephrine as needed. These drugs cause vasoconstriction, retarding the release of the chemical mediators into the tissues from the blood stream. This reduces hyperemia, chemosis and other symptoms.
Mast cell stabilizers such as Alomide and Crolom help prevent the onset of allergic reactions by blocking the adherence of the IgE-allergen compound to the mast cell. Treat patients with a history of recurrent seasonal allergies using a mast cell stabilizer q.i.d. for four weeks in advance of allergy season. Patanol (olopatadine 0.1%) combines mast cell stabilization with an antihistamine to offer therapy that is for both acute and chronic symptoms. The effects last eight hours, allowing for b.i.d. rather than q.i.d. dosing.
In moderate to severe cases, recommend one or more of the following, used from two to four times per day as needed: a topical medication such as Patanol or Livostin, oral antihistamines such as Benadryl, or a topical non-steroidal anti-inflammatory drug (Acular, Voltaren or Profenal). In extremely symptomatic cases, use a topical steroid such as Vexol, Flarex or Alrex q.i.d.
Only prostaglandins and thromboxanes are produced when cyclooxygenase interacts with arachidonic acid. Leukotrienes, by contrast, are produced from the break-down of arachido
Senile Entropion
Signs and Symptoms
Entropion is defined as inversion of the eyelid margin. The phenomenon may occur unilaterally or bilaterally. Although it may involve the upper or lower eyelid, the lower lids are affected more frequently. Clinical features associated with entropion may be observed both in and out of the biomicroscope and include in-turning of the eyelid margin, eyelid skin or eyelashes contacting the cornea creating ocular irritation, foreign body sensation, epiphora, conjunctival hyperemia, superficial punctate epitheliopathy and, in severe or untreated cases, corneal ulceration.
Pathophysiology
Etiologically, there are four classifications of entropion: senile (or involutional), congenital, cicatricial, and spastic.
Senile entropion is considered to be the most common form. The lower eyelid turns toward the globe because of increased horizontal lid laxity, an over-riding preseptal orbicularis, disinserted or atrophied lid retractors or tendons, and involutional enophthalmos.
Congenital entropion typically effects the upper eyelid and results from structural defects in the tarsal plate, shortened posterior lamellae (tarsal plate and conjunctiva), or eyelid retractor dysgenesis. Epiblepharon (a fold of skin that overlaps the eyelid margin pushing the eyelid margin inward), prominent epicanthus (a fold of skin partially covering the inner canthus, caruncle and plica semiluminaris) and microophthalmos are factors as well.
Cicatricial entropion is produced when there is as a vertical shortening of the tarsus secondary to scarring of ocular tissue brought about by disorders such as Stevens-Johnson syndrome, ocular cicatricial pemphigoid, trachoma, herpes zoster, trauma, chemical injuries, or thermal burns.
Spastic entropion occurs secondarily to neurologic, inflammatory or irritative processes of the eyelids. Blepharospasm and involutional changes following surgery are among the common sources.
Management
While the treatment of choice should be guided by the underlying cause, the fundamental philosophies of management include moving the lid margins and lashes away from the cornea and lubricating and providing antibiotic coverage for a compromised epithelium. Generally, copious artificial tear drops and ointments can be combined with bacitracin or erythromicin ointment, b.i.d. to q.i.d., in all cases.
Solutions for senile or involutional entropion includes eyelid retraction via taping, thermal cautery or Quickert suture placement (a 2 to 3mm double nylon suture placed into the eyelid 2 to 3mm below the lid margin, perpendicular to the lid margin causing the lid to rotate away from the cornea). Other more complicated surgical solutions exist and should referred to the ocular plastic surgeon. Botulinum toxin injection has been demonstrated as a highly effective alternative to lid taping for temporary eyelid reposition in patients awaiting surgery.
In cicatricial cases, surgical repair may include excision of the scar with a tarsal plate graft from preserved sclera, ear cartilage or hard palate (in most severe circumstances) along with conjunctival and mucous membrane grafting using fetal amniotic membrane tissue.
The easiest way to resolve spastic entropion is to remove the offending irritant. In cases that involve the seventh cranial nerve (essential blepharospasm, orofacial dyskinesia, hemifacial spasm, facial myokymia) a neuro-ophthalmic consult is indicated. In some instances these conditions can be managed pharmacologically using anti-seizure medications.
Congenital cases rarely improve on their own and almost always require surgical correction. In cases such as these, a specialist with experience in pediatric oculoplastics is preferred.
Clinical Pearls
A thorough history should be completed on all patients with entropion. Take note of previous eye surgery, trauma, chemical injury, chronic infection and changes in eyelid tonus.
Diagnose entropion by examining the tonus of the eyelid. A sagging lower lid margin, a positive snap back test (the eyelid is loose and snaps back poorly when pulled away from the globe), loose medial and lateral canthal tendons, and an unusually deep inferior fornix indicate the potential for lid to globe congruity problems.
The differential diagnosis of entropion includes eyelash anomalies such as trichiasis (inward turning of the cilia) and distichiasis (multiple rows of eyelashes), neuro-ophthalmic blepharospasm, traumatic etiologies, scarring from chemical injuries, and lid malposition secondary to previous ocular surgeries.
Entropion is defined as inversion of the eyelid margin. The phenomenon may occur unilaterally or bilaterally. Although it may involve the upper or lower eyelid, the lower lids are affected more frequently. Clinical features associated with entropion may be observed both in and out of the biomicroscope and include in-turning of the eyelid margin, eyelid skin or eyelashes contacting the cornea creating ocular irritation, foreign body sensation, epiphora, conjunctival hyperemia, superficial punctate epitheliopathy and, in severe or untreated cases, corneal ulceration.
Pathophysiology
Etiologically, there are four classifications of entropion: senile (or involutional), congenital, cicatricial, and spastic.
Senile entropion is considered to be the most common form. The lower eyelid turns toward the globe because of increased horizontal lid laxity, an over-riding preseptal orbicularis, disinserted or atrophied lid retractors or tendons, and involutional enophthalmos.
Congenital entropion typically effects the upper eyelid and results from structural defects in the tarsal plate, shortened posterior lamellae (tarsal plate and conjunctiva), or eyelid retractor dysgenesis. Epiblepharon (a fold of skin that overlaps the eyelid margin pushing the eyelid margin inward), prominent epicanthus (a fold of skin partially covering the inner canthus, caruncle and plica semiluminaris) and microophthalmos are factors as well.
Cicatricial entropion is produced when there is as a vertical shortening of the tarsus secondary to scarring of ocular tissue brought about by disorders such as Stevens-Johnson syndrome, ocular cicatricial pemphigoid, trachoma, herpes zoster, trauma, chemical injuries, or thermal burns.
Spastic entropion occurs secondarily to neurologic, inflammatory or irritative processes of the eyelids. Blepharospasm and involutional changes following surgery are among the common sources.
Management
While the treatment of choice should be guided by the underlying cause, the fundamental philosophies of management include moving the lid margins and lashes away from the cornea and lubricating and providing antibiotic coverage for a compromised epithelium. Generally, copious artificial tear drops and ointments can be combined with bacitracin or erythromicin ointment, b.i.d. to q.i.d., in all cases.
Solutions for senile or involutional entropion includes eyelid retraction via taping, thermal cautery or Quickert suture placement (a 2 to 3mm double nylon suture placed into the eyelid 2 to 3mm below the lid margin, perpendicular to the lid margin causing the lid to rotate away from the cornea). Other more complicated surgical solutions exist and should referred to the ocular plastic surgeon. Botulinum toxin injection has been demonstrated as a highly effective alternative to lid taping for temporary eyelid reposition in patients awaiting surgery.
In cicatricial cases, surgical repair may include excision of the scar with a tarsal plate graft from preserved sclera, ear cartilage or hard palate (in most severe circumstances) along with conjunctival and mucous membrane grafting using fetal amniotic membrane tissue.
The easiest way to resolve spastic entropion is to remove the offending irritant. In cases that involve the seventh cranial nerve (essential blepharospasm, orofacial dyskinesia, hemifacial spasm, facial myokymia) a neuro-ophthalmic consult is indicated. In some instances these conditions can be managed pharmacologically using anti-seizure medications.
Congenital cases rarely improve on their own and almost always require surgical correction. In cases such as these, a specialist with experience in pediatric oculoplastics is preferred.
Clinical Pearls
A thorough history should be completed on all patients with entropion. Take note of previous eye surgery, trauma, chemical injury, chronic infection and changes in eyelid tonus.
Diagnose entropion by examining the tonus of the eyelid. A sagging lower lid margin, a positive snap back test (the eyelid is loose and snaps back poorly when pulled away from the globe), loose medial and lateral canthal tendons, and an unusually deep inferior fornix indicate the potential for lid to globe congruity problems.
The differential diagnosis of entropion includes eyelash anomalies such as trichiasis (inward turning of the cilia) and distichiasis (multiple rows of eyelashes), neuro-ophthalmic blepharospasm, traumatic etiologies, scarring from chemical injuries, and lid malposition secondary to previous ocular surgeries.
Orbital Cellulitis
SIGNS AND SYMPTOMS
The patient with orbital cellulitis may be of any age or sex. There will be noticeable lid edema and redness, distention, proptosis, and significant pain upon palpation. Additionally, there will be diplopia from extraocular motility limitations. There typically will be a precipitating factor such as penetrating lid trauma, mucormycosis, orbital medial wall blow-out fracture, severe lid infectious disease, bite wounds, meningitis, sinusitis and sinus infection, septicemia, ketoacidosis, or dental abscess. Vision loss and an afferent pupil defect may often be present. The patient will also be systemically ill and have a fever.
PATHOPHYSIOLOGY
Orbital cellulitis results from microbial infection with subsequent inflammation of the post-septal aspect of the eyelids. The most common routes of infection are from adjacent sinuses or teeth, and direct inoculation through penetrating lid injury. Common organisms include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Haemophilus influenzae in children. There is significant potential morbidity and even mortality as a post-septal lid infection can spread through a valveless venous system leading to cavernous sinus thrombosis, meningitis, intracranial infection, and septicemia.
Inflammatory proptosis develops due to intraorbital abscesses of mucopurulent material. Ophthalmoplegia develops as a result of toxic myopathy and soft tissue edema. Vision loss will occur due to intraorbital increase in pressure from the mucopurulent abscess, compressing the optic nerve.
MANAGEMENT
Differentiate orbital cellulitis from pre-septal cellulitis so as to recognize a medical emergency. There are many superficial similarities between the two diseases, namely lid edema and redness, and pronounced pain upon palpation. However, orbital cellulitis manifests proptosis and extraocular muscle restriction, whereas pre-septal cellulitis does not. Also, patients with orbital cellulitis have fever and typically manifest decreased vision; these features are not present in pre-septal cellulitis.
Often, the degree of proptosis in orbital cellulitis cannot be readily appreciated due to the extreme lid edema. For this reason, CT scans are necessary, not only to identify orbital abscesses, but also to ascertain precipitating sinus involvement.
There is no place for topical or oral antibiotic therapy in the management of orbital cellulitis. Optimal management involves immediate consultation with and referral to a primary care physician, pediatrician, or infectious disease specialist. This is especially important with children as the potential for mortality is great. The patient needs immediate hospitalization with in-patient parenteral antibiosis.
CLINICAL PEARLS
When encountering a suspected orbital cellulitis, look for precipitating factors such as sinus infection, bite wounds, dental abscess, and penetrating injury.
Orbital cellulitis is a medical emergency and requires in-patient care.
Patients with orbital cellulitis are systemically ill. The presence of fever is highly diagnostic of post-septal orbital cellulitis. Patients who are (tentatively) diagnosed with pre-septal cellulitis should be educated about the seriousness of the development of fever.
Post-septal orbital cellulitis will have motility restriction whereas pre-septal cellulitis will not.
The patient with orbital cellulitis may be of any age or sex. There will be noticeable lid edema and redness, distention, proptosis, and significant pain upon palpation. Additionally, there will be diplopia from extraocular motility limitations. There typically will be a precipitating factor such as penetrating lid trauma, mucormycosis, orbital medial wall blow-out fracture, severe lid infectious disease, bite wounds, meningitis, sinusitis and sinus infection, septicemia, ketoacidosis, or dental abscess. Vision loss and an afferent pupil defect may often be present. The patient will also be systemically ill and have a fever.
PATHOPHYSIOLOGY
Orbital cellulitis results from microbial infection with subsequent inflammation of the post-septal aspect of the eyelids. The most common routes of infection are from adjacent sinuses or teeth, and direct inoculation through penetrating lid injury. Common organisms include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Haemophilus influenzae in children. There is significant potential morbidity and even mortality as a post-septal lid infection can spread through a valveless venous system leading to cavernous sinus thrombosis, meningitis, intracranial infection, and septicemia.
Inflammatory proptosis develops due to intraorbital abscesses of mucopurulent material. Ophthalmoplegia develops as a result of toxic myopathy and soft tissue edema. Vision loss will occur due to intraorbital increase in pressure from the mucopurulent abscess, compressing the optic nerve.
MANAGEMENT
Differentiate orbital cellulitis from pre-septal cellulitis so as to recognize a medical emergency. There are many superficial similarities between the two diseases, namely lid edema and redness, and pronounced pain upon palpation. However, orbital cellulitis manifests proptosis and extraocular muscle restriction, whereas pre-septal cellulitis does not. Also, patients with orbital cellulitis have fever and typically manifest decreased vision; these features are not present in pre-septal cellulitis.
Often, the degree of proptosis in orbital cellulitis cannot be readily appreciated due to the extreme lid edema. For this reason, CT scans are necessary, not only to identify orbital abscesses, but also to ascertain precipitating sinus involvement.
There is no place for topical or oral antibiotic therapy in the management of orbital cellulitis. Optimal management involves immediate consultation with and referral to a primary care physician, pediatrician, or infectious disease specialist. This is especially important with children as the potential for mortality is great. The patient needs immediate hospitalization with in-patient parenteral antibiosis.
CLINICAL PEARLS
When encountering a suspected orbital cellulitis, look for precipitating factors such as sinus infection, bite wounds, dental abscess, and penetrating injury.
Orbital cellulitis is a medical emergency and requires in-patient care.
Patients with orbital cellulitis are systemically ill. The presence of fever is highly diagnostic of post-septal orbital cellulitis. Patients who are (tentatively) diagnosed with pre-septal cellulitis should be educated about the seriousness of the development of fever.
Post-septal orbital cellulitis will have motility restriction whereas pre-septal cellulitis will not.
Herpex Simplex Blepharitis
SIGNS AND SYMPTOMS
Signs and Symptoms: Herpes simplex virus (HSV) infections involving the lid may present in one of two forms. The classic appearance involves an accumulation of small vesicles or pustules along the lid margin and/or periocular skin. These lesions typically have an inflamed, erythematous base. Within the first week of infection, the vesicles may ulcerate or harden into crusts.
A second “erosive-ulcerative” form of HSV blepharitis has also been described. This presentation is characterized by erosions of the lid at the Gray line or ulcers along the lid margin, or a combination of both. The lid typically displays generalized swelling and redness associated with these lesions.
HSV blepharitis is encountered primarily in children, although adults may also manifest this disorder. Presenting symptoms include pain and tenderness upon palpation, as well as increased lacrimation in severe cases. If the conjunctiva is involved, tarsal follicles may be observed along with bulbar injection and chemosis. Swollen pre-auricular nodes (pre-auricular lymphadenopathy) on the involved side is common.
PATHOPHYSIOLOGY
Herpes simplex is actually the most common virus found in humans. A member of the Herpetoviridae family, HSV is a double-stranded DNA virus that replicates within cell nuclei. As it leaves the host cell, it becomes encapsulated and can lie dormant for extended periods. Several trigger factors, including fever, trauma, emotional stress, menstruation, exogenous immunosuppressive agents, and overexposure to UV radiation can activate the virus. Transmission typically occurs by direct contact with an open epithelial lesion or contaminated bodily secretions. Rarely, the virus may be spread by contaminated materials such as towels or tissues.
Primary ocular infections occur most often in children between the ages of 6 months and 5 years, and almost invariably present as blepharitis or blepharoconjunctivitis. In recurrent attacks, the virus usually reappears as a dendritic keratitis. Several reports of recurrent HSV blepharitis have been reported in the literature, however.
MANAGEMENT
There is no specific treatment for HSV blepharitis, and most often the course of the disease is self-limiting. The use of warm saline compresses with a topical drying agent (e.g. 70% alcohol) is usually sufficient to palliate the patient. If the lesions are extensive, concomitant use of topical antibiotic ointment is prudent to prevent a secondary opportunistic bacterial infection. The use of topical or oral antiviral agents has not been proven to enhance the recovery of patients with HSV blepharitis, although it is advocated by some practitioners for more severe cases. However, topical trifluridine (Viroptic 1%) is absolutely indicated in cases presenting with corneal involvement.
The use of topical steroids on HSV lid lesions may be unwise, particularly if there is other ocular involvement. Although corticosteroids may be used without fear in cases of herpes zoster (HZO) blepharitis, their use in cases of HSV infection may predispose the patient to the eruption of a dendritic keratitis.
CLINICAL PEARLS
• Always include HZO in the differential diagnosis of HSV blepharitis. Keep in mind, however, that HZO typically affects elderly patients over the age of 70. Younger patients who present with HZO are often immunocompromised secondary to disorders such as AIDS or lymphoma. HSV blepharitis is usually encountered in children, but can occur at any age.
• Although herpes simplex is known as a sexually transmitted disease, the vast majority of ocular herpes infections are not contracted via sexual contact. This is very important to recognize when considering pediatric cases of HSV blepharitis.
Signs and Symptoms: Herpes simplex virus (HSV) infections involving the lid may present in one of two forms. The classic appearance involves an accumulation of small vesicles or pustules along the lid margin and/or periocular skin. These lesions typically have an inflamed, erythematous base. Within the first week of infection, the vesicles may ulcerate or harden into crusts.
A second “erosive-ulcerative” form of HSV blepharitis has also been described. This presentation is characterized by erosions of the lid at the Gray line or ulcers along the lid margin, or a combination of both. The lid typically displays generalized swelling and redness associated with these lesions.
HSV blepharitis is encountered primarily in children, although adults may also manifest this disorder. Presenting symptoms include pain and tenderness upon palpation, as well as increased lacrimation in severe cases. If the conjunctiva is involved, tarsal follicles may be observed along with bulbar injection and chemosis. Swollen pre-auricular nodes (pre-auricular lymphadenopathy) on the involved side is common.
PATHOPHYSIOLOGY
Herpes simplex is actually the most common virus found in humans. A member of the Herpetoviridae family, HSV is a double-stranded DNA virus that replicates within cell nuclei. As it leaves the host cell, it becomes encapsulated and can lie dormant for extended periods. Several trigger factors, including fever, trauma, emotional stress, menstruation, exogenous immunosuppressive agents, and overexposure to UV radiation can activate the virus. Transmission typically occurs by direct contact with an open epithelial lesion or contaminated bodily secretions. Rarely, the virus may be spread by contaminated materials such as towels or tissues.
Primary ocular infections occur most often in children between the ages of 6 months and 5 years, and almost invariably present as blepharitis or blepharoconjunctivitis. In recurrent attacks, the virus usually reappears as a dendritic keratitis. Several reports of recurrent HSV blepharitis have been reported in the literature, however.
MANAGEMENT
There is no specific treatment for HSV blepharitis, and most often the course of the disease is self-limiting. The use of warm saline compresses with a topical drying agent (e.g. 70% alcohol) is usually sufficient to palliate the patient. If the lesions are extensive, concomitant use of topical antibiotic ointment is prudent to prevent a secondary opportunistic bacterial infection. The use of topical or oral antiviral agents has not been proven to enhance the recovery of patients with HSV blepharitis, although it is advocated by some practitioners for more severe cases. However, topical trifluridine (Viroptic 1%) is absolutely indicated in cases presenting with corneal involvement.
The use of topical steroids on HSV lid lesions may be unwise, particularly if there is other ocular involvement. Although corticosteroids may be used without fear in cases of herpes zoster (HZO) blepharitis, their use in cases of HSV infection may predispose the patient to the eruption of a dendritic keratitis.
CLINICAL PEARLS
• Always include HZO in the differential diagnosis of HSV blepharitis. Keep in mind, however, that HZO typically affects elderly patients over the age of 70. Younger patients who present with HZO are often immunocompromised secondary to disorders such as AIDS or lymphoma. HSV blepharitis is usually encountered in children, but can occur at any age.
• Although herpes simplex is known as a sexually transmitted disease, the vast majority of ocular herpes infections are not contracted via sexual contact. This is very important to recognize when considering pediatric cases of HSV blepharitis.
Dacryocystitis
SIGNS AND SYMPTOMS
Pain, redness and swelling over the inner aspect of the lower eyelid and epiphora may signify aggravated blepharitis, meibomianitis or canaliculitis. However, suspect dacryocystitis if the problem recurs and is associated with fever and severe erythematous swelling around the nasal aspect of the lower lid; or if it involves the lacrimal sac such that mucopurulent discharge can be expressed from the inferior punctum. Older patients are predisposed to the condition as the lacrimal drainage system loses its elasticity and thins, and tears fail to flush debris through the complex. Patients with poor hygiene are at greater risk.
PATHOPHYSIOLOGY
The primary etiology of dacryocystitis is nasolacrimal obstruction secondary to mucocele of the lacrimal sac, which is precipitated by chronic blockage of the interosseous or intermembranous nasolacrimal duct. Most cases of nasolacrimal duct obstruction are found in the older population, and result from chronic mucosal degeneration, ductile stenosis, stagnation of tears, and bacterial overgrowth. Infantile dacryocystitis is uncommon but presents with the same signs and symptoms.
Lacrimal sac obstructions often produce signs and symptoms similar to dacryocystitis but not as severe. They are collectively known as canaliculitis. These infections are differentiated by solid concretions called dacryoliths, which can be expressed from the infected lacrimal sac. Dacryoliths can result from bacterial, fungal or viral infections.
MANAGEMENT
Management of an afebrile child with dacryocystitis includes oral amoxicillin/clavulanate (Augmentin) 20-40mgs/kg/day, PO, TID, or oral cefaclor 20-40mgs/kg/day, PO, TID, along with topical antibiotic drops QID (e.g. Polytrim, Tobrex, Ocuflox), ointments BID, warm compresses and acetaminophen. Management of an adult afebrile patient includes cephalexin (Keflex) or Augmentin 500mgs PO, QID along with topical antibiotic drops, ointments, warm compresses and aspirin or ibuprofen for pain and inflammation, as needed. Manage febrile patients with extreme caution. Patients who are acutely ill should be hospitalized and placed on IV cefazolin (Ancef), Q8H along with the other modalities. Consider neuroimaging (CT or MRI) when the etiology is in question.
Dacryoliths should be removed with curettage or canaliculotomy, cultured and treated accordingly with both topical and oral antibiotic, antiviral or antifungal preparations.
CLINICAL PEARLS
Obstruction of the tear drainage system can occur at any age. Punctal or canalicular stenosis may develop from a myriad of conditions. Punctal stenosis may result from conjunctival diseases such as Steven's-Johnson syndrome (dry eye and dry mouth secondary to reaction to sulfa medicine), ocular cicatricial pemphigoid, and mechanical, thermal or chemical injury. In the young, congenital anomalies of the nasolacrimal system include dacryostenosis, dacryocystocele and canalicular fistula
Bloody tears with a history of medial canthal mass should heighten suspicion for space occupying lesions. Facial cellulitis and acute ethmoidal or frontal sinusitis are among the important differential diagnoses.
Prompt, decisive and aggressive management is essential. Hospitalization with intravenous antibiotics should be considered in severe, febrile or recalcitrant presentations. Punctal dilation and nasolacrimal irrigation is always contraindicated in the acute stages. In fact, following the resolution of the acute infection, most cases remain with symptomatic epiphora, requiring dacryocystorhinostomy.
Pain, redness and swelling over the inner aspect of the lower eyelid and epiphora may signify aggravated blepharitis, meibomianitis or canaliculitis. However, suspect dacryocystitis if the problem recurs and is associated with fever and severe erythematous swelling around the nasal aspect of the lower lid; or if it involves the lacrimal sac such that mucopurulent discharge can be expressed from the inferior punctum. Older patients are predisposed to the condition as the lacrimal drainage system loses its elasticity and thins, and tears fail to flush debris through the complex. Patients with poor hygiene are at greater risk.
PATHOPHYSIOLOGY
The primary etiology of dacryocystitis is nasolacrimal obstruction secondary to mucocele of the lacrimal sac, which is precipitated by chronic blockage of the interosseous or intermembranous nasolacrimal duct. Most cases of nasolacrimal duct obstruction are found in the older population, and result from chronic mucosal degeneration, ductile stenosis, stagnation of tears, and bacterial overgrowth. Infantile dacryocystitis is uncommon but presents with the same signs and symptoms.
Lacrimal sac obstructions often produce signs and symptoms similar to dacryocystitis but not as severe. They are collectively known as canaliculitis. These infections are differentiated by solid concretions called dacryoliths, which can be expressed from the infected lacrimal sac. Dacryoliths can result from bacterial, fungal or viral infections.
MANAGEMENT
Management of an afebrile child with dacryocystitis includes oral amoxicillin/clavulanate (Augmentin) 20-40mgs/kg/day, PO, TID, or oral cefaclor 20-40mgs/kg/day, PO, TID, along with topical antibiotic drops QID (e.g. Polytrim, Tobrex, Ocuflox), ointments BID, warm compresses and acetaminophen. Management of an adult afebrile patient includes cephalexin (Keflex) or Augmentin 500mgs PO, QID along with topical antibiotic drops, ointments, warm compresses and aspirin or ibuprofen for pain and inflammation, as needed. Manage febrile patients with extreme caution. Patients who are acutely ill should be hospitalized and placed on IV cefazolin (Ancef), Q8H along with the other modalities. Consider neuroimaging (CT or MRI) when the etiology is in question.
Dacryoliths should be removed with curettage or canaliculotomy, cultured and treated accordingly with both topical and oral antibiotic, antiviral or antifungal preparations.
CLINICAL PEARLS
Obstruction of the tear drainage system can occur at any age. Punctal or canalicular stenosis may develop from a myriad of conditions. Punctal stenosis may result from conjunctival diseases such as Steven's-Johnson syndrome (dry eye and dry mouth secondary to reaction to sulfa medicine), ocular cicatricial pemphigoid, and mechanical, thermal or chemical injury. In the young, congenital anomalies of the nasolacrimal system include dacryostenosis, dacryocystocele and canalicular fistula
Bloody tears with a history of medial canthal mass should heighten suspicion for space occupying lesions. Facial cellulitis and acute ethmoidal or frontal sinusitis are among the important differential diagnoses.
Prompt, decisive and aggressive management is essential. Hospitalization with intravenous antibiotics should be considered in severe, febrile or recalcitrant presentations. Punctal dilation and nasolacrimal irrigation is always contraindicated in the acute stages. In fact, following the resolution of the acute infection, most cases remain with symptomatic epiphora, requiring dacryocystorhinostomy.
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.
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.
Subscribe to:
Posts (Atom)