Ординатура / Офтальмология / Английские материалы / Clinical Ocular Pharmacology 5th edition_Bartlett, Jaanus_2008

Made of a thermosensitive hydrophobic acrylic polymer; conforms to punctum; has no protruding cap, which prevents “rubbing out” of plug

Made of a hydrogel that forms a gelatinous material when in contact with tears; gel fills vertical portion of canaliculus

These plugs have a “cap” that protrudes from the punctum, which is uncomfortable and/or cosmetically displeasing to some patients

Short-term plugs are often used diagnostically before longer lasting plug insertion

omega-3 fatty acids is in reducing inflammatory events, particularly involving the ocular surface and specifically the meibomian glands. Omega-3 fatty acids are also naturally found in salmon, mackerel, herring, sardines, and walnuts.

Mucolytic Agents. Acetylcysteine, which is frequently used as a bronchial mucolytic agent in patients with cystic fibrosis, can be used topically in a weakened concentration for ophthalmic use. It is malodorous and may sting on instillation; however, this drug is fairly effective in disrupting mucous strands that are often present in patients with aqueous deficiency dry eye. It is not commercially available in an ophthalmic formulation; it must be compounded by a pharmacist.

Immunomodulatory Agents. For many years some practitioners treated severe dry eye with topical steroids;although anecdotal evidence was plentiful as to the benefit of this therapeutic strategy, it was not universally accepted because of a lack of understanding of the inflammatory nature of dry eye disease. Now, steroids and nonsteroidal anti-inflammatory agents are much more frequently used in the treatment of dry eye, particularly at initial diagnosis.

Cyclosporine A 0.05% (Restasis) is another immunomodulatory agent that has an excellent safety profile, even when used over a period of months or years. This treatment has been in widespread use in veterinary care since the 1970s. It has been shown to significantly improve the ocular signs and symptoms of dry eye disease, with a very

low incidence of adverse effects. This drug does not provide full therapeutic benefit when initially instilled; patients may have to wait up to a full month, or sometimes even longer, before noticing the full benefit. It is strongly recommended that during the first month of use an additional treatment modality be prescribed, such as a mild steroid plus copious artificial tears.

EVALUATION AND MANAGEMENT OF THE LACRIMAL DRAINAGE SYSTEM

Epiphora

Epiphora (spilling of tears over the lid margin) can be congenital or acquired and is one of the most common symptoms in lacrimal system disorders. If a patient complains of epiphora, dry eye syndrome should be excluded before a formal evaluation of the lacrimal drainage system, including Schirmer testing, because dry eyes can prompt reflex tearing, and a true hypersecretion disorder, although rare, also results in epiphora If the lacrimal secretory system is intact, then testing of the drainage system should be pursued.

Congenital epiphora usually results from a failure of the valve of Hasner to completely open by the time of birth.This defect is often termed congenital NLD obstruction and may be present in up to 6% of infants. Infants with NLD obstruction display epiphora, and many may have a concurrent secondary dacryocystitis (see below) as a result of the stagnated tears in the lacrimal sac.

430 CHAPTER 24 Diseases of the Lacrimal System

In these cases it may be difficult to distinguish NLD obstruction from neonatal conjunctivitis.A large percentage of infants have a spontaneous resolution of incomplete canalization of the lacrimal drainage system within the first weeks to months of life. Others may require intervention.Typically, the hydrostatic technique, or “massage,” is attempted before more invasive procedures. This massage technique relies on the hydrostatic pressure of the tears present within the drainage system to help rupture Hasner’s membrane.

It is important to understand that the volume of tears within the lacrimal sac and NLD is quite small; to maximize the effect of the massage technique it is imperative that both the upper and lower puncta be gently held closed with one finger while the other hand is used to gently trace the area of the lacrimal sac and NLD in a downward motion (Figure 24-12). If the puncta are not occluded during this technique, any external pressure applied to the drainage apparatus is released in the path of least resistance. Because in these cases there is a known obstruction distally, the effects of the pressure would be directed proximally or back in the direction of the puncta.

When properly performed this method can be very effective in rupturing Hasner’s membrane. In cases resistant to the massage technique, the clinician may attempt forceful lacrimal irrigation, probing with a flexible lacrimal probe, balloon catheter dilation, or silicone intubation. These procedures, especially the latter two, are done under general anesthesia and are typically considered only after the child reaches at least 3 to 4 months of

age; many practitioners delay surgery until 21 months due to the high likelihood of spontaneous resolution within this period.

In adults, complaints of “excessive tearing” or watering should prompt the clinician to note the blink rate and amplitude, without the patient’s knowledge that he or she is being observed for these characteristics. For the tear pump to function effectively, a full blink excursion must be made at an appropriate rate. As mentioned previously, neither the upper nor the lower puncta should be visible without lid manipulation; if the puncta are visible, it is likely that the epiphora is caused, at least in part, by poor punctal positioning. When the lids are moved so that the puncta can be evaluated, the puncta should be patent (open) and free of debris and purulent material. The lid margins should be even and regular, with no obstructions to the normal flow of tears along the tear lake. Next, gentle digital pressure should be applied at the area of the canaliculi and lacrimal sac.The presence of mucopurulent material from the puncta is indicative of canaliculitis and/or dacrycyostitis, which is discussed in the next section.

If no cause for epiphora is evident, an evaluation of the remainder of the lacrimal drainage system should be performed. This sequence of analysis is collectively known as Jones testing. To perform these tests, the minimum equipment required is a lacrimal punctal dilator (Figure 24-13) and a lacrimal irrigation apparatus, consisting of a 2- to 5-ml syringe fitted with a 23-gauge cannula (Figure 24-14). Depending on the patient’s needs, a fine Bowman’s probe and a nasal speculum may also be needed (Figure 24-15).

The Jones No. 1 and Jones No. 2 test is an evaluation of the ability of the tears to pass through the lacrimal drainage apparatus under normal physiologic conditions. It is conducted as follows:

1.NaFl is instilled into the eye (NaFl strips may be used, but many practitioners recommend that one drop of 2% liquid NaFl be used instead).

Figure 24-12 Hydrostatic massage technique for congenital nasolacrimal duct obstruction.The puncta are held gently closed with one finger while the area over the lacrimal drainage apparatus is gently massaged downward.

Figure 24-13 Lacrimal dilators (Storz, Inc., St. Louis, MO, USA). Top dilator is the Muldoon instrument; note the medium tip and rapid expansion.The next two are different sizes of the Wilder dilator. The bottom dilator is the Reudemann. It has a very fine tip and narrow taper, rendering it perhaps the most useful of the group.

Figure 24-14 Lacrimal cannulae. (Top) The 23-gauge West cannula. The shaft is straight and approximately 25 mm long. The tip is blunt, with a needle hole in the side. (Bottom) Reinforced 23-gauge cannula and syringe.

2.The patient is instructed to sit quietly without forcefully blinking.

3.After 5 minutes the clinician notes the amount of NaFl dye that remains in and around the ocular surface and adnexa.

If there is a significant amount of dye still present, it is

assumed that the lacrimal drainage system is not properly functioning. If very little or no fluorescein is present in and around the eye, it may be assumed that the fluorescein drained with the tears in the normal fashion (i.e., through the lacrimal drainage system). To confirm this finding, the patient can be asked to open his or her mouth and the clinician can look in the back of the throat for fluorescein. The use of a Burton lamp or other blue filter light source may enhance visibility of the fluorescein, but it is not mandatory. Alternatively, the patient can clear his or her nose onto a white tissue by

Figure 24-15 Bowman probes.

holding the opposite nasal opening closed and forcefully blowing onto the tissue. In either method the presence of fluorescein confirms a patent lacrimal drainage system. The absence of fluorescein with either of these two tests prompts further evaluation.

Many practitioners at this stage proceed directly to Jones II testing, with the assumption that there is an obstruction in the lacrimal drainage system beyond (i.e., more distal to) the punctal opening. However, before attempting Jones II, some practitioners require further efforts to demonstrate evidence of fluorescein within the nasolacrimal drainage system.To accomplish this, the patient may be asked to forcefully gather mucus from the nose and nasopharynx and then expel the mucus onto a white tissue. If no fluorescein is seen, the practitioner can then anesthetize the area under the inferior meatus with topical Xylocaine, and then swab this area using a thin wire probe tipped with cotton or calcium alginate.

If negative results are found with these two tests, Jones II testing is performed.

The procedure for the Jones II test is as follows:

1.Residual fluorescein is rinsed from the eye.The punctal area is anesthetized using a cotton swab soaked in a topical anesthetic, such as proparacaine.The swab is left in place for 30 to 60 seconds, during which time the patient remains sitting upright.

2.The syringe of the lacrimal irrigation apparatus is filled with sterile saline.

3.The lower punctum is dilated using a punctal dilator. The insertion of the dilator or probe is facilitated by pulling the lid slightly down and away from the nose and twisting the probe clockwise and counterclockwise. Once past the punctal opening, the probe is inserted approximately 2 mm in a vertical direction, and then it is turned nasally for a few more millimeters until whitening or “blanching” is seen at the punctal opening (Figure 24-16).

4.The dilator is then removed and the lacrimal irrigation apparatus is inserted, again respecting the anatomic configuration of the canaliculus.

5.The patient is asked to place his or head forward, with chin on or near chest, with a collection basin (white in color or lined with a white tissue) underneath the nose and mouth (Figure 24-17).

6.The clinician then attempts to inject a small amount (1 to 2 ml) of saline into the punctum by depressing the plunger on the syringe.

There are three possible outcomes to Jones No. 1 and

Jones No. 2 testing:

1.No fluid exits the system; a complete obstruction exists within the drainage apparatus. Usually, it is impossible to inject any fluid into the system at the time of testing due to the complete blockage (i.e., no fluid goes in, no fluid comes out).

2.Fluid is injected into the lower punctum but regurgitates through the upper punctum. The fluid may be mixed with mucopurulent material and/or

432 CHAPTER 24 Diseases of the Lacrimal System

A

B

Figure 24-16 Procedure for lower punctal dilation. (A) The dilator is inserted vertically approximately 2 mm. (B) It is then brought near the horizontal plane of the lower eyelid. The lower lid can be gently pulled laterally to straighten the canaliculus. (Courtesy Richard J. Clompus, O.D.)

blood, indicating infection or a possible neoplasm, respectively.

3.Fluorescein-stained fluid exits the nose; this indicates a partial distal (farther away from the punctum) obstruction. Occasionally, the obstruction is composed of a bolus of mucopurulent material that is dislodged by the force of the irrigation. In these cases the irrigation procedure itself is therapeutic, and often the epiphora disappears immediately. Other cases may require surgical intervention to maintain the patency of the lower lacrimal drainage system (dacryocystorhinostomy).

If clear fluid is expelled from the nose without any fluo-

rescein present, it is likely that rather than a true obstruction of the lacrimal drainage system a punctal stenosis or ectropion is the culprit.This diagnosis can be assumed by the fact that no fluorescein ever entered the drainage system during the Jones I test, in contrast to the situation where fluorescein enters the system but gets lodged deep within the drainage apparatus (scenario 3 above).

Figure 24-17 Secondary dye test (Jones No. 2 test). Lacrimal lavage. Patient is seated and inclined forward for irrigation. Note basin to catch effluent. (Reprinted with permission from Semes L, Melore GG. Dilation and diagnostic irrigation of the lacrimal drainage system. J Am Optom Assoc 1986; 57:518–525.)

DIAGNOSIS AND MANAGEMENT OF LACRIMAL DRAINAGE DISORDERS

Punctal Disorders

Etiology

Occlusion of the lacrimal puncta is called atresia when congenital and stenosis when it is acquired. Each produces true epiphora, although congenital cases tend to produce fewer clinical signs and symptoms than do acquired cases.

Stenosis of the punctum can be secondary to allergy, infection, trauma, or simply the result of aging-associated loss of collagen and elastin tone. The latter is the most frequent cause of acquired epiphora.

Punctal ectropion is the result of eyelid ectropion. Causes include mechanical (e.g., excess weight on the lid as the result of a lid growth), cicatricial (resulting from scar tissue formation), congenital, age-related, and allergic.

Management

In some cases of punctal occlusion, the dilation and irrigation procedures are at least temporarily therapeutic; redilation of the lacrimal punctum may need to be performed on a semiregular basis to ensure continued comfort. Often, patients with mild degrees of punctal ectropion can be satisfactorily managed by instructing the patient to manually reposition the eyelid at regular intervals throughout the day.

If these methods are ineffective, surgery may be required. Procedures to repair the punctum are referred to as punctoplasty.

If the punctum is involuted such that it cannot be identified or opened, dacryocystorhinostomy may be required.This surgical procedure shunts the tears around lacrimal drainage obstructions into the nasal cavity.

Canalicular Disorders

Etiology

Canaliculitis, or infection and inflammation within the canaliculus, is a relatively rare disorder. Obstruction of the canaliculi may also result from surgery, trauma, and neoplastic disorders.

Diagnosis

Typical patient complaints with canaliculitis include a smoldering usually unilateral red eye that has been resistant to antibiotic therapy. Epiphora may or may not be a primary symptom. An important clinical sign in the diagnosis of canalicular obstruction has been termed the wrinkle sign. When a “soft stop” is encountered during lacrimal probing or irrigation, the clinician can observe compression of the medial canthal skin (wrinkling) in the presence of canalicular obstruction. This is in contrast to the presentation in normal patients, where the visualization of smooth skin and unobstructed advancement of the instrument to the lacrimal bone are present (i.e., “hard stop”), indicating a patent proximal drainage system. The “soft stop” can be caused by bacterial colonization or more frequently by stones, or dacryoliths, forming within the canaliculus.

Common causative organisms in adults with canaliculitis include Staphylococcus aureus and Actinomyces species. Primary herpetic infections (herpes simplex, varicella, and vaccinia) have a higher prevalence among patients younger than age 20 years and often present with cutaneous manifestations of the infectious disease. Chronic allergies may also be associated with canalicular obstruction. Occasionally, patients may suffer from canalicular obstruction as a result of topical antimetabolite treatment such as 5-fluorouracil or mitomycin C.

Management

Some mild cases of canalicular obstruction can be temporarily or permanently “cured” with the dilation and irrigation procedure. However, this is the exception rather than the rule.

Because of the antibiotic resistance of many subspecies of Staphylococcus, it is recommended that culture and sensitivity studies of any purulent material be undertaken to maximize the chance for successful treatment of canaliculitis. Antibiosis should be directed at the specific causative organism isolated. Systemic penicillin is usually recommended in treating actinomyces, in addition to topical penicillin.

Success in eradicating the infection also depends on removal of concretions and purulent material from the involved canaliculi. Actinomyces species are especially problematic in this regard, often forming casts within the canaliculus. These particles make it exceedingly difficult to treat cases of bacterial canaliculitis with topical medications alone; in general, these dacryoliths must be removed before successful antibiotic treatment. In a few cases manual expression of the stones or casts is possible; in others, canaliculotomy is required. In very resistant cases dacryocystorhinostomy may be necessary.

Herpetic canaliculitis should be treated using standard treatment protocols, including oral antiviral agents. Periodic dilation and irrigation of the lacrimal drainage system may enhance the chance for successful recanalization, though there is a risk of scar tissue formation with repeated dilation and irrigation procedures.

Relief of allergic canalicular obstruction may be managed with topical medications, but these cases, as well as drug-induced canalicular obstruction, may require dacryocystorhinostomy procedures.

Acquired Dacryocystitis

Etiology

When a patient older than 1 year has swelling over the lacrimal sac, the swelling most often results from acquired dacryocystitis. Culture studies usually identify

Staphylococcus aureus, Staphylococcus epidermidis, and

Pseudomonas species as the offending organisms in adults. Cases of methicillin-resistant S. aureus have been detected, along with a trend toward a relatively higher prevalence of gram-negative organisms as compared with gram-positive bacteria, with Haemophilus influenzae a potential pathogen in children. As with canaliculitis, culture studies of any purulent material present are highly recommended, because many other uncommon pathogens have been reported in this disorder. It should be noted, however, that results from culture studies may take several days and in some cases yield no growth.

Faced with a chronic dacryocystitis, the clinician needs to be aware of masquerade syndromes. Epithelial carcinomas and malignant lymphoma have been reported from histologic and immunohistochemical analysis, respectively, of biopsies of the lacrimal sac taken at dacryocystorhinostomy. Rhabdomyosarcoma has also been identified. Displaced silicone plugs have been found as potential vectors for infection not only in the lacrimal sac but also in other areas of the lacrimal drainage route.

434 CHAPTER 24 Diseases of the Lacrimal System

Diagnosis

The swelling characteristic of dacryocystitis is limited in its upward extent by the medial canthal tendon. Mucoceles and solid tumor masses may extend above the tendon and masquerade as dacryocystitis. Pain and hyperemia are consistent features of infectious dacryocystitis, whereas mucoceles and tumors are often painless.

Management

Daily massage over the area of the lacrimal sac, with or without the application of hot compresses, is critical to empty the infected contents of the sac. If the patient is afebrile, broad-spectrum antibiotics, such as Augmentin or a second-generation cephalosporin, should be prescribed for 10 to 14 days. Antimicrobial therapy should be directed at the causative organism identified in culture studies, if available. Some practitioners recommend daily irrigation of the lacrimal drainage apparatus with topical antibiotics, because this has been reported to help focus the drug in the area of highest bacterial colonization. After resolution of the infection, diagnostic dilation and irrigation should be carried out to determine the necessity for surgical repair.

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Disorders of the conjunctiva are one of the leading causes of unscheduled visits to eye care practitioners. A wide range of etiologies for conjunctival disease exists, including infection, inflammation, trauma, degeneration, and neoplasm. Dermatologic conditions and systemic diseases may also affect the conjunctiva. Despite this broad variety of possible etiologies, the clinical response of the conjunctiva is relatively limited. This narrow range of possible presentations can sometimes make diagnosis of conjunctival disorders challenging for the clinician.

Advances have been made in the diagnosis and management of conjunctival disease. These advances include new medications, new diagnostic techniques, and better understanding of the management of what is often a deceptively simple disorder. These new developments ease the diagnostic burden and improve treatment efficacy for the clinician.

ANATOMY OF THE CONJUNCTIVA

The conjunctiva is a mucous membrane that lines the inner portions of the eyelids and is reflected onto the globe, overlying the episclera and anterior sclera to the limbus.The membrane consists of normally nonkeratinized epithelium overlying a substantia propria or stroma containing connective tissue and a vascular network. Anatomically and clinically, the conjunctiva consists of three distinct sections: palpebral or tarsal conjunctiva, fornix conjunctiva, and bulbar conjunctiva (Figure 25-1). The conjunctiva develops embryologically from surface ectoderm, along with the epidermis of the eyelid, corneal epithelium, and lens epithelium. This common derivation provides an anatomic basis for the clinical association of conjunctivitis with dermatologic conditions of the eyelids as well as certain systemic diseases.

Palpebral Conjunctiva

The palpebral conjunctiva begins at the posterior eyelid margin and extends posteriorly toward the fornix.

The keratinized epithelium of the eyelids gradually transforms into the moist mucous membrane of the conjunctiva. The palpebral conjunctiva adheres tightly to the tarsus over the entire superior eyelid, as compared with the loosely adherent inferior palpebral conjunctiva. Clinically, this anatomic variation contributes to the different appearance of papillary hypertrophy occurring in the superior versus inferior palpebral conjunctiva.

The palpebral conjunctiva is composed of nonkeratinized stratified epithelium that decreases in thickness as it proceeds from the eyelid margin. Many mucin-secreting goblet cells are located near the fornix. The epithelium overlies the substantia propria, which consists of delicate connective tissue and blood vessels. Most of the immune system cellular components reside in the substantia propria.The stroma contains lymphocytes, lymphoid follicles, neutrophils, plasma cells, and mast cells, all of which proliferate extensively in conjunctival inflammatory disease.This proliferation leads to the formation of papillae and follicles.

Fornix Conjunctiva

The conjunctival fornix extends over the globe, beginning and ending at the medially located plica semilunaris and caruncle. The fornix adheres loosely to the underlying stroma. A small fold or folds in the fornix conjunctiva permit free motion during eye movements. The lower fornix contains an abundance of lymphoid follicles and inflammatory cells. The accessory lacrimal glands of Krause are located in the superior fornix, with few accessory lacrimal glands situated in the lower fornix.

Bulbar Conjunctiva

The conjunctiva proceeds onto the globe from the fornix to form the bulbar conjunctiva, which overlies Tenon’s capsule and merges with the limbal cornea. Loosely attached to the capsule over the entire globe, the bulbar conjunctiva forms a homogeneous layer of stratified squamous epithelium at the limbus and contains many goblet

438 CHAPTER 25 Diseases of the Conjunctiva

Fornix

Bulbar conjunctiva

Eyelid

Palpebral (Tarsal) conjunctiva

Cornea

Figure 25-1 Anatomic division of the conjunctiva.

cells near the fornix. Stratified squamous epithelium is notable for its ability to bear friction and shearing forces that might occur from lid action during the blink. The goblet cells secrete mucopolysaccharides that form the mucin layer of the tear film. Loss of goblet cells may result in various forms of ocular surface disease, ranging from dry eye syndrome to cicatricial disorders. There is evidence that the conjunctival epithelium also produces mucin. The limbal conjunctival substantia propria contains many sensitive unmyelinated nerve fibers and free nerve endings as well as a complex network of perilimbal vessels and vascular arcades. Medially, the bulbar conjunctiva is bordered by the caruncle, which forms a mucocutaneous junction between the bulbar conjunctiva and the epidermis of the skin. Accessory lacrimal glands may occasionally be located in the caruncle.

A substantial concentration of Langerhans cells exists at the limbus. These cells, also known as monocytes within the blood and macrophages when deposited in tissues, derive from bone marrow and have a dendritic morphologic shape. They occur within all epithelial surfaces and mucous membranes. Langerhans cells initiate the ocular immune response by functioning as anti- gen-presenting cells. Foreign antigens displayed on their surfaces are recognized by T lymphocytes in a complex interaction.

MICROBIOLOGIC FEATURES

OF THE CONJUNCTIVA

Normal Flora

At birth, infants emerge from a sterile environment to be almost immediately exposed to an environment filled with a wide variety of microbes. The conjunctiva, as with

other mucous membranes, normally sustains permanent flora of indigenous bacteria.These organisms constitute a protective host defense that helps prevent pathogens from multiplying efficiently by competing with them for resources. Normal flora shifts with age, physical state of the host, and local environmental factors.Adults normally harbor a greater number of species than do children. Children typically have significantly higher numbers of Streptococcus species, whereas adults have higher numbers of anaerobic species, predominantly Propionibacterium. Long-term contact lens wearers show higher numbers of bacterial species, whereas short-term contact lens wear appears to cause no significant alteration in microbial flora.

Normal flora may become pathogenic in immunocompromised or debilitated patients and in cases where epithelial barrier disturbances and immune compromise retardation exposes the conjunctiva or cornea to infection. Compromised host defenses, such as reductions in tear lactoferrin levels, may be a factor. Viruses and parasites, although often present in asymptomatic individuals, are not considered part of the normal flora. Several studies have documented the similarity between the normal flora of the conjunctiva and that of the upper respiratory tract and eyelid skin. The primary microbial organisms retrieved from normal uninfected eyes are

Staphylococcus epidermidis, Staphylococcus aureus, and

Corynebacterium species (diphtheroids). At least one of these organisms could be isolated from 61% of the specimens from 92 healthy eyes during repetitive cultures of the conjunctiva. S. epidermidis was most commonly found. Other organisms found on a transient basis include Streptococcus pneumoniae, the viridans group of streptococci, Haemophilus influenzae, and Pseudomonas aeruginosa. Occasionally, even enteric gram-negative rods such as Escherichia coli are detected. Obligate gram-positive rod anaerobes are isolated in 50% of the eyes cultured.

Propionibacterium acnes, commonly isolated from the skin, is the most frequently found anaerobe. Factors and conditions such as blepharitis, dry eye syndrome, meibomian gland dysfunction, and contact lens use may influence the composition of the normal flora or cause disruption to normal epithelial microbial barriers, either of which can lead to disease in susceptible patients. Although immunocompromised individuals may harbor Candida albicans, fungi are considered opportunistic pathogens. Little evidence supports the existence of any indigenous fungi in the normal conjunctival flora.

Common Microbial Pathogens

Almost any microbial organism can cause infectious conjunctivitis.The infectious organisms include bacteria, chlamydia, fungi, and viruses. In immunocompetent persons the primary causes of conjunctivitis are bacteria and viruses in children younger than 12 years and viruses

Box 25-1 Causes of Infectious Conjunctivitis

Bacterial

Gram positive

Staphylococcus aureus

Staphylococcus epidermidis

Streptococcus pneumoniae

Streptococcus pyogenes

Corynebacterium diphtheriae

Gram negative

Haemophilus influenzae

Neisseria gonorrhoeae

Escherichia coli

Pseudomonas aeruginosa

Proteus mirabilis

Moraxella lacunata

Moraxella catarrhalis

Viral

Adenovirus

Herpes simplex

Varicella-zoster

Molluscum contagiosum

Enterovirus 70

Epstein-Barr

Chlamydial

Chlamydia trachomatis

Fungal

Candida albicans

Aspergillus species

in adults and children older than 12 years of age. The primary bacterial pathogens are S. aureus, H. influenzae, and S. pneumoniae.

Adenovirus and herpes simplex virus (HSV) are the most common causes of viral conjunctivitis. The frequency of infection by one of these organisms varies depending on the particular region’s climate and other environmental factors. Box 25-1 summarizes the most significant ocular infectious agents.

INFLAMMATION OF THE CONJUNCTIVA

Several distinct clinical signs herald conjunctival inflammation. However, the actual presentation depends on the nature of the causative agent, the time course, and any preexisting disease. Conjunctival tissue may be exposed to antigens, pathogens, toxins, or irritants through airborne transmission; direct contact (hand to eye, person to person, or from contaminated instruments or surfaces); and inadvertent sexual transmission.

Systemic disorders may also manifest with conjunctival inflammation. Acute or chronic conjunctivitis may present with any of five signs of conjunctival inflammation: chemosis, hyperemia, discharge or exudate, follicles, and papillae (Table 25-1). Specific patterns of inflammation may be helpful in diagnosis of the underlying cause.

All immune system inflammatory cells may be elicited in extraordinary numbers in conjunctival tissues. Lymphocytes, neutrophils, mast cells, and plasma cells are present from birth and increase in quantity with age and antigenic exposure. Lymphoid tissue, however, is not present at birth but develops within the first few months of life. Increased vascular permeability, resulting from the ocular immune response to antigens, infectious agents, toxins, or other environmental stimuli (e.g., smoke or wind), often results in hyperemia, chemosis, or exudative discharge. The severity of the clinical presentation depends on both the causative agent and type of immune response. When present, conjunctival discharge may be serous, mucoid, purulent, fibrinous, or hemorrhagic.

Conjunctival membranes and pseudomembranes consist of fibrin and cellular debris.True membranes are attached firmly to the underlying conjunctival epithelium such that when removed, the underlying epithelium is stripped away, leaving an abraded bleeding surface. Pseudomembranes are similar in composition to true membranes but do not adhere to the underlying epithelium, making their removal less traumatic. Clinically, the distinction may be difficult to ascertain. Removal is indicated when the membranes interfere with the healing process or are a source of irritation.True membranes and pseudomembranes are associated with specific causes, and their presence can be helpful in establishing a differential diagnosis.

Papillary hypertrophy represents a nonspecific inflammatory response of the conjunctiva most commonly observed in allergic or bacterial conjunctivitis. It is due to cellular infiltration of the substantia propria by inflammatory cells, including eosinophils, lymphocytes, mast cells, and polymorphonuclear leukocytes. Papillary hypertrophy produces elevations of the conjunctival epithelium and stroma termed papillae, which have a delineating margin and contain a small central vascular tuft. This central vessel is the source of cellular infiltration. Papillae vary in size from less than 1 mm to the giant cobblestone-shaped excrescences seen in contact lens–related giant papillary conjunctivitis or, more notably, in vernal keratoconjunctivitis (VKC). When the papillae are small, the conjunctiva has a grossly smooth velvety appearance.

Follicles result from focal lymphoid hyperplasia most commonly associated with chlamydial, viral, or toxic exposure, including preservatives in eyedrops or high levels of chlorine in pool water. Clinically, conjunctival follicles appear as avascular, translucent to whitish gray, amorphous nodules 0.5 to 1.5 mm in diameter, usually located in the tarsal and fornix conjunctiva. Small external