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Eye Disorders indicated. Symptoms are usually mild and resolve u'ithin 1 to 2 weeks. Failure to improve or suspicion of herpes simplex virus infection, which frequently causes eyelid lesicles. should prompt referral to an ophthalmologist. Bacterial conjunctivitis is highly contagious and com- monly spreads through direct contact. Gram-positire bacte ria are commonly implicated. Findings develop over 1 to 2 days. Cold compresses can be used for symptomatic relief. Use of topical antibacterial therapy, including trimethoprim polymyxin B or erythromycin, is associated r,r'ith earlier clinical and microbiological remission compared rt'ith pla cebo. Treatment may reduce transmissibility. Hort'erer. 65'/. of patients improve within 2 to 5 days without antibiotic therapy. Therefore, withholding antibiotics can be consid ered for patients who are not immunocompromised. do t I G U R E 7. Ihis patient has a traumatic hyphema, which is recognized by the not wear contact lenses, and do not work in health layered blood level in the anterior chamber of the eye.Traumatic hyphema is a care facilities. common complication of blunt or penetrating injury to the eye and can result in Neisserio gonorrhoeoe causes hyperacute bacterial vision loss. Large hyphema collections can be delected with a penlight; smaller collections of blood require evaluation with a slit lamp. conjunctivitis, characterized by sudden onset of symptoms with rapid progression to vision loss (Figrrre 8). Emergent ophthalmologr referral, hospitalization, and both systemic should be initiated immediately, with emergent referral to and topical antimicrobials are indicated. ophthalmologz. Allergic conjunctivitis can be seasonal or perennial and is Vision threatening eye infections requiring immediate characterized by clear watery discharge, bilateral eye pruritus. intravenous antibiotics and ophthalmologic evaluation include and redness and is accompanied by other allergic symptoms, endophthalmitis (particularly bacterial infection of the aque including rhinorrhea. Treatment involves removing the ous and vitreous humors) and orbital cellulitis (infection of the offending agent when possible. along with use of either topical fat and muscle cells of the orbit). Preseptal cellulitis (periorbi antihistamines or mast-cell inhibitors. tal cellulitis) is an inf'ection of the anterior portion of the eyelid Suspected conjunctivitis occurring in the context of that rarely leads to serious complications. Both conditions contact lens use should prompt consideration of keratitis. result in eyelid swelling, erythema, and pain, but only orbital Contact lens use should be discontinued until redness and cellulitis causes proptosis, ophthalmoplegia, and pain with eye discharge resolve completely. movement. Keratitis Keratitis is inflammation of the corneal epithelium and super Red Eye ficial stroma. It is most commonly due to bacterial infection Cardinal features of conditions that cause red eye are listed in (especially Pseudomonas species) in contact lens wearers but Table 56. Assessment begins by determining unilateral or can also be caused by viral infections, such as herpes simplex bilateral involvementl symptom duration; and the presence or absence of trauma, discharge, pain, photophobia, and visual changes. History of previous similar episodes, contact lens use, and medical history are also important to elicit. Examination should include assessment of visual acuity, pupillary size and light response, redness pattem and location, and palpation of preauricular lymph nodes.

indicated. Symptoms are usually mild and resolve u'ithin 1 to 2 weeks. Failure to improve or suspicion of herpes simplex virus infection, which frequently causes eyelid lesicles. should prompt referral to an ophthalmologist. Bacterial conjunctivitis is highly contagious and com- monly spreads through direct contact. Gram-positire bacte ria are commonly implicated. Findings develop over 1 to 2 days. Cold compresses can be used for symptomatic relief. Use of topical antibacterial therapy, including trimethoprim polymyxin B or erythromycin, is associated r,r'ith earlier clinical and microbiological remission compared rt'ith pla cebo. Treatment may reduce transmissibility. Hort'erer. 65'/. of patients improve within 2 to 5 days without antibiotic therapy. Therefore, withholding antibiotics can be consid ered for patients who are not immunocompromised. do t I G U R E 7. Ihis patient has a traumatic hyphema, which is recognized by the not wear contact lenses, and do not work in health layered blood level in the anterior chamber of the eye.Traumatic hyphema is a care facilities. common complication of blunt or penetrating injury to the eye and can result in Neisserio gonorrhoeoe causes hyperacute bacterial vision loss. Large hyphema collections can be delected with a penlight; smaller collections of blood require evaluation with a slit lamp. conjunctivitis, characterized by sudden onset of symptoms with rapid progression to vision loss (Figrrre 8). Emergent ophthalmologr referral, hospitalization, and both systemic should be initiated immediately, with emergent referral to and topical antimicrobials are indicated. ophthalmologz. Allergic conjunctivitis can be seasonal or perennial and is Vision threatening eye infections requiring immediate characterized by clear watery discharge, bilateral eye pruritus. intravenous antibiotics and ophthalmologic evaluation include and redness and is accompanied by other allergic symptoms, endophthalmitis (particularly bacterial infection of the aque including rhinorrhea. Treatment involves removing the ous and vitreous humors) and orbital cellulitis (infection of the offending agent when possible. along with use of either topical fat and muscle cells of the orbit). Preseptal cellulitis (periorbi antihistamines or mast-cell inhibitors. tal cellulitis) is an inf'ection of the anterior portion of the eyelid Suspected conjunctivitis occurring in the context of that rarely leads to serious complications. Both conditions contact lens use should prompt consideration of keratitis. result in eyelid swelling, erythema, and pain, but only orbital Contact lens use should be discontinued until redness and cellulitis causes proptosis, ophthalmoplegia, and pain with eye discharge resolve completely. movement. Keratitis Keratitis is inflammation of the corneal epithelium and super Red Eye ficial stroma. It is most commonly due to bacterial infection Cardinal features of conditions that cause red eye are listed in (especially Pseudomonas species) in contact lens wearers but Table 56. Assessment begins by determining unilateral or can also be caused by viral infections, such as herpes simplex bilateral involvementl symptom duration; and the presence or absence of trauma, discharge, pain, photophobia, and visual changes. History of previous similar episodes, contact lens use, and medical history are also important to elicit. Examination should include assessment of visual acuity, pupillary size and light response, redness pattem and location, and palpation of preauricular lymph nodes. Conjunctivitis Conjunctivitis is the most common cause of red eye and can be due to infectious or noninfectious etiologies. Viral conjunctivitis is commonly spread through direct contact and often occurs concomitantly with upper respira tory tract infection. Adenovirus, coxsackievirus, and enterovi rus are frequently implicated pathogens. Symptoms typically start in one eye before spreading bilaterally. Therapy is sup F I G U R E 8. Hyperacute bacterial conjunctivitis due to Neisseria gonorrhoeae portive and includes cold compresses; antibiotics are not demonstrating copious purulent drainage and conjunctival swelling.

Conjunctivitis Conjunctivitis is the most common cause of red eye and can be due to infectious or noninfectious etiologies. Viral conjunctivitis is commonly spread through direct contact and often occurs concomitantly with upper respira tory tract infection. Adenovirus, coxsackievirus, and enterovi rus are frequently implicated pathogens. Symptoms typically start in one eye before spreading bilaterally. Therapy is sup F I G U R E 8. Hyperacute bacterial conjunctivitis due to Neisseria gonorrhoeae portive and includes cold compresses; antibiotics are not demonstrating copious purulent drainage and conjunctival swelling. 68

Eye Disorders Cause Symptoms Visual Changes Examination Associated Immediate Findings Systemic Ophthalmologic Conditiong Evaluation Viral conjunctivitis lrritation only; Typically no Diffuse erythema Findings consistent No associated with changes, although of conjunctiva; with viral upper watery discharge discharge may periauricular respiratory tract and crusting cloud vision adenopathy infection Bacterial lrritation only; Typically no Mucopurulent None No conjunctivitis associated with changes, although discharge with mucopurulent discharge may eyelash debris and discharge cloud vision eyelid matting Hyperacute Sudden onset of May progress to Diffusely bright red None Yes bacterial copious purulent visual changes/loss conjunctiva with conjunctivitis discharge with copious purulent (Neisseria significant pain discharge gonorrhoeae) Keratitis Severe eye Blurred/diminished Corneal stromal None Yes discomfort, with vision infiltrates; difficulty keeping circumferential the affected eye redness around the open; often border of the sclera accompanied by and cornea (ciliary foreign-body flush') sensation Episcleritis Rapid onset of eye None Localized or diffuse Minority of patients No redness and superficial redness have underlying tenderness; of episcleral vessels disease occasional watery and episclera (rheumatoid discharge arthritis, inflammatory bowel disease) Scleritis Severe pain, often Decreased vision; Diffuse or nodular Rheumatologic Yes worse with eye may be complete scleral edema with disease movement; loss red/violaceous (rheumatoid associated tearing discoloration; arthritis, vasculitis) and photophobia globe tenderness in >50% of patients Uveitis/iritis Eye redness and Variable; may Hyperemia Common; infection Yes pain; photophobia include floaters surrounding the (HSV CMV); limbus (ciliary inflammatory flushu); hypopyon; disorders pupil constriction (spondyloarthritis, with decreased sarcoidosis) light reactivity Subconjunctival Mild or none None Discrete bright red Spontaneous; No hemorrhage confluent region in setting of without hyperemia anticoag u lation; trauma; increased pressure (coughing)

Cause Symptoms Visual Changes Examination Associated Immediate Findings Systemic Ophthalmologic Conditiong Evaluation Viral conjunctivitis lrritation only; Typically no Diffuse erythema Findings consistent No associated with changes, although of conjunctiva; with viral upper watery discharge discharge may periauricular respiratory tract and crusting cloud vision adenopathy infection Bacterial lrritation only; Typically no Mucopurulent None No conjunctivitis associated with changes, although discharge with mucopurulent discharge may eyelash debris and discharge cloud vision eyelid matting Hyperacute Sudden onset of May progress to Diffusely bright red None Yes bacterial copious purulent visual changes/loss conjunctiva with conjunctivitis discharge with copious purulent (Neisseria significant pain discharge gonorrhoeae) Keratitis Severe eye Blurred/diminished Corneal stromal None Yes discomfort, with vision infiltrates; difficulty keeping circumferential the affected eye redness around the open; often border of the sclera accompanied by and cornea (ciliary foreign-body flush') sensation Episcleritis Rapid onset of eye None Localized or diffuse Minority of patients No redness and superficial redness have underlying tenderness; of episcleral vessels disease occasional watery and episclera (rheumatoid discharge arthritis, inflammatory bowel disease) Scleritis Severe pain, often Decreased vision; Diffuse or nodular Rheumatologic Yes worse with eye may be complete scleral edema with disease movement; loss red/violaceous (rheumatoid associated tearing discoloration; arthritis, vasculitis) and photophobia globe tenderness in >50% of patients Uveitis/iritis Eye redness and Variable; may Hyperemia Common; infection Yes pain; photophobia include floaters surrounding the (HSV CMV); limbus (ciliary inflammatory flushu); hypopyon; disorders pupil constriction (spondyloarthritis, with decreased sarcoidosis) light reactivity Subconjunctival Mild or none None Discrete bright red Spontaneous; No hemorrhage confluent region in setting of without hyperemia anticoag u lation; trauma; increased pressure (coughing) C[/V = cytomegalovirus; HSV = herpes simplex virus.

Cause Symptoms Visual Changes Examination Associated Immediate Findings Systemic Ophthalmologic Conditiong Evaluation Viral conjunctivitis lrritation only; Typically no Diffuse erythema Findings consistent No associated with changes, although of conjunctiva; with viral upper watery discharge discharge may periauricular respiratory tract and crusting cloud vision adenopathy infection Bacterial lrritation only; Typically no Mucopurulent None No conjunctivitis associated with changes, although discharge with mucopurulent discharge may eyelash debris and discharge cloud vision eyelid matting Hyperacute Sudden onset of May progress to Diffusely bright red None Yes bacterial copious purulent visual changes/loss conjunctiva with conjunctivitis discharge with copious purulent (Neisseria significant pain discharge gonorrhoeae) Keratitis Severe eye Blurred/diminished Corneal stromal None Yes discomfort, with vision infiltrates; difficulty keeping circumferential the affected eye redness around the open; often border of the sclera accompanied by and cornea (ciliary foreign-body flush') sensation Episcleritis Rapid onset of eye None Localized or diffuse Minority of patients No redness and superficial redness have underlying tenderness; of episcleral vessels disease occasional watery and episclera (rheumatoid discharge arthritis, inflammatory bowel disease) Scleritis Severe pain, often Decreased vision; Diffuse or nodular Rheumatologic Yes worse with eye may be complete scleral edema with disease movement; loss red/violaceous (rheumatoid associated tearing discoloration; arthritis, vasculitis) and photophobia globe tenderness in >50% of patients Uveitis/iritis Eye redness and Variable; may Hyperemia Common; infection Yes pain; photophobia include floaters surrounding the (HSV CMV); limbus (ciliary inflammatory flushu); hypopyon; disorders pupil constriction (spondyloarthritis, with decreased sarcoidosis) light reactivity Subconjunctival Mild or none None Discrete bright red Spontaneous; No hemorrhage confluent region in setting of without hyperemia anticoag u lation; trauma; increased pressure (coughing) C[/V = cytomegalovirus; HSV = herpes simplex virus. 'Ciliary flush is a violet hue surrounding and circumferential to the cornea due to dilated episcleral and deep conjunctival vessels.

Cause Symptoms Visual Changes Examination Associated Immediate Findings Systemic Ophthalmologic Conditiong Evaluation Viral conjunctivitis lrritation only; Typically no Diffuse erythema Findings consistent No associated with changes, although of conjunctiva; with viral upper watery discharge discharge may periauricular respiratory tract and crusting cloud vision adenopathy infection Bacterial lrritation only; Typically no Mucopurulent None No conjunctivitis associated with changes, although discharge with mucopurulent discharge may eyelash debris and discharge cloud vision eyelid matting Hyperacute Sudden onset of May progress to Diffusely bright red None Yes bacterial copious purulent visual changes/loss conjunctiva with conjunctivitis discharge with copious purulent (Neisseria significant pain discharge gonorrhoeae) Keratitis Severe eye Blurred/diminished Corneal stromal None Yes discomfort, with vision infiltrates; difficulty keeping circumferential the affected eye redness around the open; often border of the sclera accompanied by and cornea (ciliary foreign-body flush') sensation Episcleritis Rapid onset of eye None Localized or diffuse Minority of patients No redness and superficial redness have underlying tenderness; of episcleral vessels disease occasional watery and episclera (rheumatoid discharge arthritis, inflammatory bowel disease) Scleritis Severe pain, often Decreased vision; Diffuse or nodular Rheumatologic Yes worse with eye may be complete scleral edema with disease movement; loss red/violaceous (rheumatoid associated tearing discoloration; arthritis, vasculitis) and photophobia globe tenderness in >50% of patients Uveitis/iritis Eye redness and Variable; may Hyperemia Common; infection Yes pain; photophobia include floaters surrounding the (HSV CMV); limbus (ciliary inflammatory flushu); hypopyon; disorders pupil constriction (spondyloarthritis, with decreased sarcoidosis) light reactivity Subconjunctival Mild or none None Discrete bright red Spontaneous; No hemorrhage confluent region in setting of without hyperemia anticoag u lation; trauma; increased pressure (coughing) C[/V = cytomegalovirus; HSV = herpes simplex virus. 'Ciliary flush is a violet hue surrounding and circumferential to the cornea due to dilated episcleral and deep conjunctival vessels. virus and adenovirus. Diminished vision and severe eye dis- systemic NSAIDs for symptom relief. Patients with recurrent comfort with circumferential hyperemia are tlpical (Figure 9 episodes should be evaluated for underlying disease. and Figure 10). Bacterial keratitis requires immediate ophthal- Scleritis is an inflammatory disorder of the sclera that mologic evaluation. causes severe pain and, unlike episcleritis, can threaten vision (Figure 12). Scleritis is often associated with underlying Episcleritis and Scleritis inflammatory diseases, such as rheumatoid arthritis and sys- Episcleritis is a self-limited inflammation of the episclera temic vasculitis. Diagnosis should prompt immediate referral (layer between sclera and conjunctiva) that usually resolves to an ophthalmologisti systemic glucocorticoids or immuno within several weeks (Figure l1). Treatment consists of suppressive agents are usually required for treatment.

virus and adenovirus. Diminished vision and severe eye dis- systemic NSAIDs for symptom relief. Patients with recurrent comfort with circumferential hyperemia are tlpical (Figure 9 episodes should be evaluated for underlying disease. and Figure 10). Bacterial keratitis requires immediate ophthal- Scleritis is an inflammatory disorder of the sclera that mologic evaluation. causes severe pain and, unlike episcleritis, can threaten vision (Figure 12). Scleritis is often associated with underlying Episcleritis and Scleritis inflammatory diseases, such as rheumatoid arthritis and sys- Episcleritis is a self-limited inflammation of the episclera temic vasculitis. Diagnosis should prompt immediate referral (layer between sclera and conjunctiva) that usually resolves to an ophthalmologisti systemic glucocorticoids or immuno within several weeks (Figure l1). Treatment consists of suppressive agents are usually required for treatment. 69

Eye Disorders t I G U R E 9. Bacterial keratitis typically presents with a red eye; photophobia; pain or foreign body sensation; and a corneal opacity or infiltrate, recognized as a round white spot at 1 otlock in this image. FIGU RE 1 1 . Episcleritis showing superficial dilated blood vessels with white sclera visible between the blood vessels.

t I G U R E 9. Bacterial keratitis typically presents with a red eye; photophobia; pain or foreign body sensation; and a corneal opacity or infiltrate, recognized as a round white spot at 1 otlock in this image. FIGU RE 1 1 . Episcleritis showing superficial dilated blood vessels with white sclera visible between the blood vessels. FIGU RE 1 0, Chronic stromal corneal infiltrates in patient with adenoviral or picornaviral keratitis. tIGURE 1 2. The cardinal sign of scleritis is edema of the sclera, often associated with a violaceous discoloration of the globe (red arow). Tenderness is invariably present. Iypically, there is intense dilation of the episcleral blood vessels (yellow arrowl.Scleral inflammation may be focal or diffuse. Uveitis Uveitis is inflammation of the iris and ciliary body. It is asso- ciated with many systemic infections and inflammatory dis Blepharitis eases (most commonly ankylosing spondylitis and reactive Blepharitis is eyelid inflammation, which may be posterior arthritis) (Figure 13). In severe cases, a hypopyon (Figure 14) or or anterior. Posterior blepharitis involves inner eyelid inflam purulent material accumulation in the anterior eye chamber mation near the meibomian glands. Posterior blepharitis can may be observed. Patients with uveitis require immediate occur in patients with rosacea and seborrheic dermatitis. In referral to an ophthalmologist. anterior blepharitis, inflammation occurs at the eyelid bases. Eyelid colonization with staphylococcal species, contact der Subconjunctival Hemorrhage matitis, and psoriasis may be involved. Subconjunctival hemorrhages result from ruptured sub Findings may include eyelid swelling, redness, and skin conjunctival blood vessels due to intense coughing, flaking; eyelash loss, misdirection, and crusting; and excessive vomiting, and minor trauma. They are asymptomatic and tearing (Figure 16). Corneal erosions and ulcerations can be usually resolve within several weeks (Figure 15). No treat- seen in severe cases. Treatment of all forms of blepharitis ment is necessary. involves warm compresses, eyelid washing and massage, and

FIGU RE 1 0, Chronic stromal corneal infiltrates in patient with adenoviral or picornaviral keratitis. tIGURE 1 2. The cardinal sign of scleritis is edema of the sclera, often associated with a violaceous discoloration of the globe (red arow). Tenderness is invariably present. Iypically, there is intense dilation of the episcleral blood vessels (yellow arrowl.Scleral inflammation may be focal or diffuse. Uveitis Uveitis is inflammation of the iris and ciliary body. It is asso- ciated with many systemic infections and inflammatory dis Blepharitis eases (most commonly ankylosing spondylitis and reactive Blepharitis is eyelid inflammation, which may be posterior arthritis) (Figure 13). In severe cases, a hypopyon (Figure 14) or or anterior. Posterior blepharitis involves inner eyelid inflam purulent material accumulation in the anterior eye chamber mation near the meibomian glands. Posterior blepharitis can may be observed. Patients with uveitis require immediate occur in patients with rosacea and seborrheic dermatitis. In referral to an ophthalmologist. anterior blepharitis, inflammation occurs at the eyelid bases. Eyelid colonization with staphylococcal species, contact der Subconjunctival Hemorrhage matitis, and psoriasis may be involved. Subconjunctival hemorrhages result from ruptured sub Findings may include eyelid swelling, redness, and skin conjunctival blood vessels due to intense coughing, flaking; eyelash loss, misdirection, and crusting; and excessive vomiting, and minor trauma. They are asymptomatic and tearing (Figure 16). Corneal erosions and ulcerations can be usually resolve within several weeks (Figure 15). No treat- seen in severe cases. Treatment of all forms of blepharitis ment is necessary. involves warm compresses, eyelid washing and massage, and 70

Eye Disorders t I G U R E 1 3. Uveitis is an inflammation of the uvea that commonly presents as a red eye with pain, photophobia, and blurred vision. Anterior uveitis is inflammation of the iris and ciliary body. lritis is synonymous with anterior uveitis, but if the ciliary body is involved the correct term is iridocyclitis. Anterior uveitis is characterized by circumferential redness (ciliary flush) at the corneal limbus (junction ol the cornea and sclera). ln some cases, adhesions may develop between F I G UR E 1 6. The most obvious signs of blepharitis are redness and stickiness the iris and the lens, which may distort the normal roundness of the pupil. of the eyelid, with clumping of scaly skin around the base of the eyelashes. use ofartificial tears. Refractory cases necessitate referral to an ophthalmologist.

t I G U R E 1 3. Uveitis is an inflammation of the uvea that commonly presents as a red eye with pain, photophobia, and blurred vision. Anterior uveitis is inflammation of the iris and ciliary body. lritis is synonymous with anterior uveitis, but if the ciliary body is involved the correct term is iridocyclitis. Anterior uveitis is characterized by circumferential redness (ciliary flush) at the corneal limbus (junction ol the cornea and sclera). ln some cases, adhesions may develop between F I G UR E 1 6. The most obvious signs of blepharitis are redness and stickiness the iris and the lens, which may distort the normal roundness of the pupil. of the eyelid, with clumping of scaly skin around the base of the eyelashes. use ofartificial tears. Refractory cases necessitate referral to an ophthalmologist. . Conjunctivitis is the most common cause of red eye and can have a viral, bacterial, or allergic etiolory; all types are associated with ocular discharge. . Keratitis is an ocular emergenry that represents inflam- mation of the cornea and is characterized by diminished vision and severe eye discomfort with circumferential hyperemia. o Episcleritis is a self-limited inflammation of the epi- sclera; scleritis is a painful inflammatory disorder of the sclera that can threaten vision. t I G U R E 1 4. A hypopyon is recognized as a layered collection o{ pus (arows) in the anterior chamber. o Blepharitis is eyelid inflammation; treatment involves eyelid hygiene (warm compresses, eyelid washing, and massage) and use ofartificial tears.

. Conjunctivitis is the most common cause of red eye and can have a viral, bacterial, or allergic etiolory; all types are associated with ocular discharge. . Keratitis is an ocular emergenry that represents inflam- mation of the cornea and is characterized by diminished vision and severe eye discomfort with circumferential hyperemia. o Episcleritis is a self-limited inflammation of the epi- sclera; scleritis is a painful inflammatory disorder of the sclera that can threaten vision. t I G U R E 1 4. A hypopyon is recognized as a layered collection o{ pus (arows) in the anterior chamber. o Blepharitis is eyelid inflammation; treatment involves eyelid hygiene (warm compresses, eyelid washing, and massage) and use ofartificial tears. Dry Eye Dry eye (keratoconjunctivitis sicca) is a multifactorial inflam- matory disorder and results from abnormal eye lubrication. Normal tear film consists of an aqueous component formed by lacrimal glands, lipids produced by meibomian glands, and mucins produced by conjunctival goblet cells. Abnormalities in any component of the film can lead to dry eyes. In most cases, ocular surface inflammation additionallyplays a central role. Systemic medications, such as p-blockers, antihista mines, antipsychotics, and antineoplastics, can also cause dry eye. FIGURE 15. Subconjunctival hemonhageischaracterizedbyunilateral, localized, $rmptoms are uzually bilateral and include ocular pain, for- and sharply circumscribed redness without discharge or pain. eigrr body sensation, light sensitivity, tearing, irritation/redness, I I

Dry Eye Dry eye (keratoconjunctivitis sicca) is a multifactorial inflam- matory disorder and results from abnormal eye lubrication. Normal tear film consists of an aqueous component formed by lacrimal glands, lipids produced by meibomian glands, and mucins produced by conjunctival goblet cells. Abnormalities in any component of the film can lead to dry eyes. In most cases, ocular surface inflammation additionallyplays a central role. Systemic medications, such as p-blockers, antihista mines, antipsychotics, and antineoplastics, can also cause dry eye. FIGURE 15. Subconjunctival hemonhageischaracterizedbyunilateral, localized, $rmptoms are uzually bilateral and include ocular pain, for- and sharply circumscribed redness without discharge or pain. eigrr body sensation, light sensitivity, tearing, irritation/redness, I I 71

Eye Disorders and fluctuating visual disturbance. Treatment includes using artificial tears and, occasionally, punctal occlusion or plugs; reducing inflammation, most commonly with topical cyclosporine; and treating eyelid disease with appropriate hygiene. Reduced screen time, increased fluid intake and ambient humidity, avoidance of environmental and medica- tion triggers, and use of protective eyewear should also be recommended. f,IY POITT . Treatment of dry eye includes artificial tears and, occa- sionally, punctal plugs; topical cyclosporine; warm compresses; and lifestyle changes (such as reduced screen time and increased fluid intake). F I G UR E I 7. A relatively large cup to disc ratio (diameter of cup/diameter of Corneal Abrasions and Ulcers disc) and cupping identified by the disappearance of vessels over the edge of the Corneal abrasions are superficial epithelial defects that result attenuated optic rim are characteristic of glaucoma.

F I G UR E I 7. A relatively large cup to disc ratio (diameter of cup/diameter of Corneal Abrasions and Ulcers disc) and cupping identified by the disappearance of vessels over the edge of the Corneal abrasions are superficial epithelial defects that result attenuated optic rim are characteristic of glaucoma. lrom mechanical trauma, foreign bodies, contact lens use, and chemical burns. Symptoms include severe eye pain, for Primary Open-Angle Glaucoma eign body sensation, light sensitivity, and tearing. Fluorescein Primary open angle glaucoma (POAG) accounts for more staining permits visualization of abrasions and should be than B0'7, of glaucoma cases in the United States. POAG is performed in all patients along with visual acuity assess characterized by decreased aqueous flow with a normal ment. Vision loss requires immediate ophthalmologr refer irido corneal angle (Figure 18). POAG is often asymptomatic ral. Pain management (acetaminophen, NSAIDs) promotes until later disease stages. Peripheral visual field loss is the proper healing. Topical antimicrobials are not necessary in earliest symptom of POAG, but it frequently goes unreported patients who do not wear contact lenses. In contact lens and progression to central vision loss occurs in untreated wearers, however, topical antibiotics with antipseudomonal patients. Once present, vision loss is permanent. Treatment activity (ciprofloxacin, ofloxacin, gentamycin, tobramycin) focuses on decreasing IOP with surgery or medications. should be given to prevent bacterial superinfection. Eye Topical medications used in the treatment of POAG are listed patches should be avoided in patients with small, uncompli- in Table 57. cated corneal abrasions. Corneal ulcers most often result from bacterial infections Angle-Closure Glaucoma and extend deeper than abrasions, exposing the underlying ln angle-closure glaucoma (ACG), a narrowed irido corneal stroma. Corneal ulcers warrant immediate referral to an angle obstructs aqueous flow (see Figure 18). ACG may be ophthalmologist. primary or secondary to a process such as posterior cham- ber hemorrhage or tumor causing irido-corneal angle clo Cataracts sure. Symptoms can develop acutely or insidiously. depend ing on the rate of IOP increase. Acute symptoms include Cataracts (lens opacification) frequently cause glare sensitivity severe eye pain, headache, nausea/vomiting, and visualiz- and vision impairment, particularly at night. Examination ing halos around lights. Eye dilation should be avoided reveals lens opaciflcation along with diminished or absent red when ACG is suspected to avoid precipitously increasing reflex. Asymptomatic cataracts require no treatment. Patients IOP. Extremely high IOPs are seen on tonometry. Acute ACG with vision-impairing cataracts should be referred for phaco- is an ocular emergency, and laser peripheral iridotomy emulsification with intraoperative lens replacement. should be performed within t hour of presentation. If iri dotomy is delayed, IOP-lowering drops should be adminis- Glaucoma trated to lower the pressure until iridotomy can be performed. Glaucoma is a group of progressive optic neuropathies charac terized by atrophy ofthe neuroretinal rim ofthe optic nerve, rEY POITTS resulting in an increased cup to disc ratio (Figure 17). Most o Primary open-angle glaucoma (POAG) is characterized but not all affected patients have increased intraocular pres- by decreased aqueous flow with a normal irido-corneal sure (lOP). Glaucoma is the second leading cause of blindness angle; visual fleld loss is often the earliest symptom of in the United States and the most common cause of blindness POAG' (continued) in Black persons.

lrom mechanical trauma, foreign bodies, contact lens use, and chemical burns. Symptoms include severe eye pain, for Primary Open-Angle Glaucoma eign body sensation, light sensitivity, and tearing. Fluorescein Primary open angle glaucoma (POAG) accounts for more staining permits visualization of abrasions and should be than B0'7, of glaucoma cases in the United States. POAG is performed in all patients along with visual acuity assess characterized by decreased aqueous flow with a normal ment. Vision loss requires immediate ophthalmologr refer irido corneal angle (Figure 18). POAG is often asymptomatic ral. Pain management (acetaminophen, NSAIDs) promotes until later disease stages. Peripheral visual field loss is the proper healing. Topical antimicrobials are not necessary in earliest symptom of POAG, but it frequently goes unreported patients who do not wear contact lenses. In contact lens and progression to central vision loss occurs in untreated wearers, however, topical antibiotics with antipseudomonal patients. Once present, vision loss is permanent. Treatment activity (ciprofloxacin, ofloxacin, gentamycin, tobramycin) focuses on decreasing IOP with surgery or medications. should be given to prevent bacterial superinfection. Eye Topical medications used in the treatment of POAG are listed patches should be avoided in patients with small, uncompli- in Table 57. cated corneal abrasions. Corneal ulcers most often result from bacterial infections Angle-Closure Glaucoma and extend deeper than abrasions, exposing the underlying ln angle-closure glaucoma (ACG), a narrowed irido corneal stroma. Corneal ulcers warrant immediate referral to an angle obstructs aqueous flow (see Figure 18). ACG may be ophthalmologist. primary or secondary to a process such as posterior cham- ber hemorrhage or tumor causing irido-corneal angle clo Cataracts sure. Symptoms can develop acutely or insidiously. depend ing on the rate of IOP increase. Acute symptoms include Cataracts (lens opacification) frequently cause glare sensitivity severe eye pain, headache, nausea/vomiting, and visualiz- and vision impairment, particularly at night. Examination ing halos around lights. Eye dilation should be avoided reveals lens opaciflcation along with diminished or absent red when ACG is suspected to avoid precipitously increasing reflex. Asymptomatic cataracts require no treatment. Patients IOP. Extremely high IOPs are seen on tonometry. Acute ACG with vision-impairing cataracts should be referred for phaco- is an ocular emergency, and laser peripheral iridotomy emulsification with intraoperative lens replacement. should be performed within t hour of presentation. If iri dotomy is delayed, IOP-lowering drops should be adminis- Glaucoma trated to lower the pressure until iridotomy can be performed. Glaucoma is a group of progressive optic neuropathies charac terized by atrophy ofthe neuroretinal rim ofthe optic nerve, rEY POITTS resulting in an increased cup to disc ratio (Figure 17). Most o Primary open-angle glaucoma (POAG) is characterized but not all affected patients have increased intraocular pres- by decreased aqueous flow with a normal irido-corneal sure (lOP). Glaucoma is the second leading cause of blindness angle; visual fleld loss is often the earliest symptom of in the United States and the most common cause of blindness POAG' (continued) in Black persons. 72

Eye Disorders Normal Abnormal Cornea Trabecular Ang e Trabecular network network I Canal of I Canal of Schlemm Normal Closed Schlemm I lris Lens - FIGURE lS.Iheanatomyoltheeye,comparingnormal withclosed-angleglaucoma.Particularattentionshouldbepaidtosizeoftheangleineyewithnormalanatomy (where it is larger) and the size of angle in patient with narrow angle due to the positioning of the iris.

Trabecular Ang e Trabecular network network I Canal of I Canal of Schlemm Normal Closed Schlemm I lris Lens - FIGURE lS.Iheanatomyoltheeye,comparingnormal withclosed-angleglaucoma.Particularattentionshouldbepaidtosizeoftheangleineyewithnormalanatomy (where it is larger) and the size of angle in patient with narrow angle due to the positioning of the iris. TABLE 57. Topical Medications Used forTreatment of rEY P0ltTS (ominued) Primary Open-Angle Glaucoma . Patients with acute-onset angle closure glaucoma pre- Medication Mechanism of Common Side sent with severe eye pain, headache, nausea/vomiting, Action Effects and visualizing halos around lights; iridotomy should o-Adrenergic Decreases Dry mouth, be performed within I hour of symptom presentation. agonists production of somnolence, (bromidine, aqueous humor hypotension, apraclonidine) conjunctivitis medicamentosa Age-Related Macular B-Blockers (betaxolol, Decreases production of Dry eye, bradycardia, bronchospasm, Degeneration carteolol, aqueous humor fatigue, depressed Age related macular degeneration (AMD) is a progressive dis levobunolol, mood ease involving the central retina that causes painless central metipranolol, vision loss. Ear$-stage AMD is characterized by drusen (lipid timolol) deposits) and retinal pigment epithelium defects. AMD is fur Carbonic Decreases Eye irritation, sour anhydrase production of taste ther classified as either wet (neovascular, exudative) or dry inhibitors aqueous humor (non-neovascular, atrophic) (Figure 19 and Figure 2o). Wet (brinzolamide, AMD can progress to blindness in weeks to months, whereas dorzolamide) dry AMD typically progresses to blindness over years to dec Cholinergic lncreases flow of Eye pain, blurred ades. Initial symptoms include distorted vision (particularly agonists aqueous humor vision, decreased (pilocarpine) through trabecular night vision, headache with reading), difficulty with facial recognition, and central network scotoma. Prostaglandin lncreases flow of Change in iris color, Smoking is the largest modifiable risk factor for AMD, analogues aqueous humor keratitis, eyelash and cessation is strongly encouraged for all patients. (bimatoprost, through lengthening, Supplementation with vitamin C, vitamin E, p carotene, zinc, latanoprost, uveoscleral periocular skin tafluprost, pathway hy pe rpig m e ntation and copper has been shown to decrease progression of AMD. travoprost, In patients who continue to smoke, lutein and zeaxanthin can unoprostone) be used in lieu of B carotene to avoid increasing the risk for Adapted from Gupta D, Chen PP Glaucoma. Am Fam Physician.2016;93:668 74. lung cancer (see Routine Care of the Healthy Patient). IPMID; 271 758391 Intravitreal injections of vascular endothelial growth factor

TABLE 57. Topical Medications Used forTreatment of rEY P0ltTS (ominued) Primary Open-Angle Glaucoma . Patients with acute-onset angle closure glaucoma pre- Medication Mechanism of Common Side sent with severe eye pain, headache, nausea/vomiting, Action Effects and visualizing halos around lights; iridotomy should o-Adrenergic Decreases Dry mouth, be performed within I hour of symptom presentation. agonists production of somnolence, (bromidine, aqueous humor hypotension, apraclonidine) conjunctivitis medicamentosa Age-Related Macular B-Blockers (betaxolol, Decreases production of Dry eye, bradycardia, bronchospasm, Degeneration carteolol, aqueous humor fatigue, depressed Age related macular degeneration (AMD) is a progressive dis levobunolol, mood ease involving the central retina that causes painless central metipranolol, vision loss. Ear$-stage AMD is characterized by drusen (lipid timolol) deposits) and retinal pigment epithelium defects. AMD is fur Carbonic Decreases Eye irritation, sour anhydrase production of taste ther classified as either wet (neovascular, exudative) or dry inhibitors aqueous humor (non-neovascular, atrophic) (Figure 19 and Figure 2o). Wet (brinzolamide, AMD can progress to blindness in weeks to months, whereas dorzolamide) dry AMD typically progresses to blindness over years to dec Cholinergic lncreases flow of Eye pain, blurred ades. Initial symptoms include distorted vision (particularly agonists aqueous humor vision, decreased (pilocarpine) through trabecular night vision, headache with reading), difficulty with facial recognition, and central network scotoma. Prostaglandin lncreases flow of Change in iris color, Smoking is the largest modifiable risk factor for AMD, analogues aqueous humor keratitis, eyelash and cessation is strongly encouraged for all patients. (bimatoprost, through lengthening, Supplementation with vitamin C, vitamin E, p carotene, zinc, latanoprost, uveoscleral periocular skin tafluprost, pathway hy pe rpig m e ntation and copper has been shown to decrease progression of AMD. travoprost, In patients who continue to smoke, lutein and zeaxanthin can unoprostone) be used in lieu of B carotene to avoid increasing the risk for Adapted from Gupta D, Chen PP Glaucoma. Am Fam Physician.2016;93:668 74. lung cancer (see Routine Care of the Healthy Patient). IPMID; 271 758391 Intravitreal injections of vascular endothelial growth factor 73

Eye Disorders I .i : FIGURE 2l.Ihefoldingandtearingoftheretinathatischaracteristicof retinal I detachment. F I G UR E I 9. Age-related macular degeneration (wet form), showing clumps of hyperpigmentation lred anow) and evidence of su breti nal hemonhage (b lack anow\. reveal other lesions. First line therapy is high-dose intrave- nous glucocorticoids. Retinal Detachment Retinal detachment involves separation of the retinal neurosen- sory layer from underlying structures and is an ocular emergenry requiring immediate referral to an ophthalmologist (Figure 21). ffiptoms include unilateral flashing lights and floaters. Risk factors include myopia, cataract surgery retinal lattice degenera tion and retinalbreaks, and positive family history

Retinal Detachment Retinal detachment involves separation of the retinal neurosen- sory layer from underlying structures and is an ocular emergenry requiring immediate referral to an ophthalmologist (Figure 21). ffiptoms include unilateral flashing lights and floaters. Risk factors include myopia, cataract surgery retinal lattice degenera tion and retinalbreaks, and positive family history 't Retinal Vascular Occlusion Retinal Artery Occlusion Central retinal artery occlusion (CRAO) presents as sudden, painless severe monocular vision loss. Occlusion of smaller branches (branch retinal artery occlusion) leads to less pro : found visual field defects. CRAO is most commonly due to FIGURE 20. Atrophic(dry)age-related maculardegeneration,showing distinct carotid artery atherosclerosis but can also be due to cardiogenic yellow-white lesions called drusen (arows) surrounding the macular area and areas embolism, thrombophilia, and giant cell arteritis. Some affected of pigment mottling. patients have a history oftransient episodes ofpainless vision loss. Fundoscopic examination may reveal retinal pallor, a inhibitors are a cornerstone ofadvanced disease treatment and "cherry red" fovea, and intemrpted blood columns within reti may improve vision or delay deterioration. nal vessels. CRAO is an ocular emergency requiring urgent referral to an ophthalmologist. fEY 'OtTI is the largest modifiable risk factor for age- o Smoking Retinal Vein Occlusion related macular degeneration. Central retinal vein occlusion (CRVO) is usually due to primary thrombus formation, whereas branch retinal vein occlusion (BRVO) is usually due to compression of a vein by adjacent Optic Neuritis arterioles. CRVO typically presents as painless, blurred Optic neuritis is a demyelinating inflammation of the optic monocular vision. BRVO may be asymptomatic or cause sco nerve and is most commonly due to multiple sclerosis. It toma or visual field defect. Examination may reveal an afferent manifests as painful acute monocular vision loss that develops pupillary defect (particularly in CRVO), retinal vein conges- over a period of hours to days. Examination may reveal papil- tion, retinal hemorrhage, and cotton-wool spots (Figure 22). litis (see MKSAP 19 Neurologz). An afferent pupillary defect is Risk factors for CRVO include advanced age, diabetes mellitus, common, as is a central scotoma on visual field testing. and hypertension. Presence of CRVO should prompt immedi- Diagnosis is clinical, although MRI may confirm diagnosis and ate referral to an ophthalmologist.

't Retinal Vascular Occlusion Retinal Artery Occlusion Central retinal artery occlusion (CRAO) presents as sudden, painless severe monocular vision loss. Occlusion of smaller branches (branch retinal artery occlusion) leads to less pro : found visual field defects. CRAO is most commonly due to FIGURE 20. Atrophic(dry)age-related maculardegeneration,showing distinct carotid artery atherosclerosis but can also be due to cardiogenic yellow-white lesions called drusen (arows) surrounding the macular area and areas embolism, thrombophilia, and giant cell arteritis. Some affected of pigment mottling. patients have a history oftransient episodes ofpainless vision loss. Fundoscopic examination may reveal retinal pallor, a inhibitors are a cornerstone ofadvanced disease treatment and "cherry red" fovea, and intemrpted blood columns within reti may improve vision or delay deterioration. nal vessels. CRAO is an ocular emergency requiring urgent referral to an ophthalmologist. fEY 'OtTI is the largest modifiable risk factor for age- o Smoking Retinal Vein Occlusion related macular degeneration. Central retinal vein occlusion (CRVO) is usually due to primary thrombus formation, whereas branch retinal vein occlusion (BRVO) is usually due to compression of a vein by adjacent Optic Neuritis arterioles. CRVO typically presents as painless, blurred Optic neuritis is a demyelinating inflammation of the optic monocular vision. BRVO may be asymptomatic or cause sco nerve and is most commonly due to multiple sclerosis. It toma or visual field defect. Examination may reveal an afferent manifests as painful acute monocular vision loss that develops pupillary defect (particularly in CRVO), retinal vein conges- over a period of hours to days. Examination may reveal papil- tion, retinal hemorrhage, and cotton-wool spots (Figure 22). litis (see MKSAP 19 Neurologz). An afferent pupillary defect is Risk factors for CRVO include advanced age, diabetes mellitus, common, as is a central scotoma on visual field testing. and hypertension. Presence of CRVO should prompt immedi- Diagnosis is clinical, although MRI may confirm diagnosis and ate referral to an ophthalmologist. 74

t t Ear, Nose, Mouth, and Throat Disorders t I L t t L t L I I t I * L t t L FIGURE 22.Centralretinalveinocclusionischaracterizedbyopticdiscswelling, L dilated and tortuous veins, and flame-shaped retinal hemorrhages (white arow) and cotton'wool spols(yellow anow) ("blood and thunder'). t L

t t L t L I I t I * L t t L FIGURE 22.Centralretinalveinocclusionischaracterizedbyopticdiscswelling, L dilated and tortuous veins, and flame-shaped retinal hemorrhages (white arow) and cotton'wool spols(yellow anow) ("blood and thunder'). t L L o Central retinal artery occlusion is an ocular emergency F I G U R E 2 3. Evidence of tympanic membrane retraction, perforation, and that presents as sudden, painless severe monocular accumulation of squamous debris consistent with cholesteatoma. t vision loss and is most commonly due to carotid artery L atherosclerosis. high-dose aspirin, and NSAIDs may cause hearing loss. Although hearing loss is associated with loop diuretics, it is o Central retinal vein occlusion typically presents as pain- L often temporary in the absence of other ototoxic medications. less blurred monocular vision, whereas branch retinal I Genetics is implicated in hearing loss and plays a role in 25% L vein occlusion may be asyrnptomatic or present with I to 50% of adult onset hearing loss. scotoma or visual field defect. t According to the U.S. Preventive Services Task Force rec- I ommendations, evidence is insufficient to assess the benefits t I and harms ol screening for hearing loss in asymptomatic i Ear, Nose, Mouth, and adults aged 50 years or older. Simple and effective tests, such as evaluating whether a patient can hear a whispered voice or 5 Throat Disorders single question screening (for example, "Do you have diffi- i culty with your hearing?"), can be performed in the office. Hearing Loss Additional in office screening maneuvers are described in t An estimated 50'/. of adults aged 60 to 69 years in the United Table 59. In patients with identified hearing loss, physical States have hearing loss that affects their day-to-day commu- examination should include otoscopic examination as well as nication. Hearing loss is underrecognized by patients and the Weber and Rinne tests (T[ble 60) to differentiate conduc- physicians and can negatively affect relationships and lead to tive from sensorineural hearing loss. Routine referral to an social isolation and reduced quality of life. It is associated with audiologist is indicated when hearing loss is identified. higher rates of unemployment, depression, dementia, hospi Imaging (typically MRI) is rarely required unless the hearing talization, falls, functional decline, and death. Ioss is acute and unilateral or associated with other neurologic Hearing loss is categorized according to the anatomic changes. Sudden-onset hearing loss (within 72 hours) requires deficit: conductive (outer or middle ear), sensorineural (inner more urgent referral to an audiologist and MRI of the retroc- ear), or mixed (Table 58). Conductive hearing loss is caused by ochlear structures. obstruction or pathologr of the outer or middle ear (such as Treatment options for hearing loss include hearing- cholesteatoma, Figure 23) that prevents sound transmission assistive devices, hearing aids, and cochlear implants. Many and is more often associated with pain or ear drainage. varieties of hearing-assistive devices exist, and they can be Sensorineural hearing loss is caused by disorders of the coch- linked with hearing aids. Examples include amplified tele- lea, auditory nerve, and central nervous system and is more phones, notification systems, personal amplifiers, and televi- often accompanied by tinnitus or vertigo. For discussion of sion streamers. Use of hearing aids is low owing to patient vertigo, see MKSAP 19 General lnternal Medicine 1. Such medi barriers that include cost, stigma, cosmetic appearance, per- cations as aminoglycosides, tetracycline, chemotherapeutic ceived ineffectiveness, and physical discomfort in wearing agents (cisplatin, carboplatin, 5 fluorouracil, bleomycin), them. Treatment of sudden sensorineural hearing loss may

L o Central retinal artery occlusion is an ocular emergency F I G U R E 2 3. Evidence of tympanic membrane retraction, perforation, and that presents as sudden, painless severe monocular accumulation of squamous debris consistent with cholesteatoma. t vision loss and is most commonly due to carotid artery L atherosclerosis. high-dose aspirin, and NSAIDs may cause hearing loss. Although hearing loss is associated with loop diuretics, it is o Central retinal vein occlusion typically presents as pain- L often temporary in the absence of other ototoxic medications. less blurred monocular vision, whereas branch retinal I Genetics is implicated in hearing loss and plays a role in 25% L vein occlusion may be asyrnptomatic or present with I to 50% of adult onset hearing loss. scotoma or visual field defect. t According to the U.S. Preventive Services Task Force rec- I ommendations, evidence is insufficient to assess the benefits t I and harms ol screening for hearing loss in asymptomatic i Ear, Nose, Mouth, and adults aged 50 years or older. Simple and effective tests, such as evaluating whether a patient can hear a whispered voice or 5 Throat Disorders single question screening (for example, "Do you have diffi- i culty with your hearing?"), can be performed in the office. Hearing Loss Additional in office screening maneuvers are described in t An estimated 50'/. of adults aged 60 to 69 years in the United Table 59. In patients with identified hearing loss, physical States have hearing loss that affects their day-to-day commu- examination should include otoscopic examination as well as nication. Hearing loss is underrecognized by patients and the Weber and Rinne tests (T[ble 60) to differentiate conduc- physicians and can negatively affect relationships and lead to tive from sensorineural hearing loss. Routine referral to an social isolation and reduced quality of life. It is associated with audiologist is indicated when hearing loss is identified. higher rates of unemployment, depression, dementia, hospi Imaging (typically MRI) is rarely required unless the hearing talization, falls, functional decline, and death. Ioss is acute and unilateral or associated with other neurologic Hearing loss is categorized according to the anatomic changes. Sudden-onset hearing loss (within 72 hours) requires deficit: conductive (outer or middle ear), sensorineural (inner more urgent referral to an audiologist and MRI of the retroc- ear), or mixed (Table 58). Conductive hearing loss is caused by ochlear structures. obstruction or pathologr of the outer or middle ear (such as Treatment options for hearing loss include hearing- cholesteatoma, Figure 23) that prevents sound transmission assistive devices, hearing aids, and cochlear implants. Many and is more often associated with pain or ear drainage. varieties of hearing-assistive devices exist, and they can be Sensorineural hearing loss is caused by disorders of the coch- linked with hearing aids. Examples include amplified tele- lea, auditory nerve, and central nervous system and is more phones, notification systems, personal amplifiers, and televi- often accompanied by tinnitus or vertigo. For discussion of sion streamers. Use of hearing aids is low owing to patient vertigo, see MKSAP 19 General lnternal Medicine 1. Such medi barriers that include cost, stigma, cosmetic appearance, per- cations as aminoglycosides, tetracycline, chemotherapeutic ceived ineffectiveness, and physical discomfort in wearing agents (cisplatin, carboplatin, 5 fluorouracil, bleomycin), them. Treatment of sudden sensorineural hearing loss may 75