Ian Pitha, Arsham Sheybani, and Linda Tsai
Introduction
Patients suffering from eye symptoms often initially present to their primary care provider. Therefore, it is important for primary care providers to feel comfortable evaluating and triaging these patients. The goal of this chapter is to familiarize primary care providers with the basics of taking an ocular history and performing a targeted ophthalmologic exam and to provide the tools needed to identify entities that can be managed in a primary care setting and those that require urgent or emergent ophthalmologic evaluation. Following a brief discussion of the ocular history and physical exam, as well as current screening recommendations, this chapter will then be organized primarily by the patient’s presenting symptom(s) and will cover etiology, symptoms, and management of each entity (see Fig. 44-1).
Figure 44-1 Rapid evaluation of ophthalmologic problems.
OCULAR HISTORY AND PHYSICAL EXAM
Careful history and examination are essential for correct diagnosis, triage (Table 44-1), and treatment of ocular conditions.
TABLE 44-1 Ophthalmology Referral Guide
History
· Correct diagnosis depends on a carefully taken, complete medical history, including past medical history, medications, family history, social history, and occupational history.
· Key elements of the ocular history are presented in Table 44-2.
· An essential initial step is to determine whether symptoms presented acutely, subacutely, or chronically.
TABLE 44-2 Elements of the Ophthalmologic History
Physical Examination
· Visual acuity
o Obtaining an accurate, best-corrected visual acuity is the most important component of the physical exam.
o Visual acuity should be tested in each eye while the patient is wearing glasses. Ideally a distance chart should be used; however, a near card can yield useful information as well.
o If formal vision charts are not available, have the patient attempt to read newspaper print or your name badge.
o If the patient cannot read the largest font on the chart, halve the distance between the patient and the chart and document the vision with “10” in the numerator (e.g., 10/200). If the patient still cannot read the chart check their ability to count fingers, or perceive hand motion or light.
o If patients do not have their glasses with them, their visual acuity when looking through a pinhole can be checked. Pinholing may resolve refractive error and is useful in the patient who cannot be optimally corrected.
· Pupillary exam
o Compare the size and shape of the pupils in light and dark conditions.
o Check for an afferent pupillary defect (APD) using the swinging flashlight test. When a light is directed from one eye to the other while the patient focuses on a distant target, the pupils should remain symmetrically constricted owing to the consensual light response. If the pupils dilate when the light is moved from the right to the left eye, then there is an APD of the left eye.
o Presence of an APD is evidence of optic nerve disease or significant retinal damage and should be evaluated in every patient presenting with vision loss.
· Ocular motility: The alignment of each eye in primary gaze, the ability of each eye to move in all directions of gaze, and the presence of nystagmus should be noted. The location of the corneal light reflex can be used to detect subtle deviations of eye position.
· Visual fields
o Have the patient cover one eye, and, while making eye contact with the patient, hold your fingers out into the four main quadrants.
o Minor field defects can be detected and documented by further visual field testing in the eye professional’s office.
· Intraocular pressure
o Intraocular pressure (IOP) is quantitatively measured in the eye professional’s office by tonometry.
o Extremely elevated IOPs, as occurs in angle-closure glaucoma, can occasionally be assessed qualitatively by palpation.
· External exam: Although most of the external exam is ideally performed using a slit lamp microscope, a penlight is useful as an initial screening tool.
· Eyelid examination
o Examine for evidence of erythema, edema, trauma, or eyelid lesions.
o Ptosis can be assessed by measuring the distance in millimeters between the corneal light reflex and the margin of the upper eyelid.
o Assess for proptosis (prominent eyes) or enophthalmos (recession of the eyeball into the orbit).
o Basal cell carcinomas affecting the eyelid most commonly develop on the lower eyelid.1
· Anterior segment examination
o The conjunctiva is the clear vascularized tissue overlying the sclera. Injection of the conjunctiva can occur in many conditions including viral and bacterial conjunctivitis.
o The cornea is the transparent, anterior wall of the outer eye. Assess the clarity of the cornea; any opacity should be characterized as diffuse or focal. Central focal opacities are more detrimental to vision than peripheral opacities.
o The anterior chamber is the fluid-filled space in between the cornea and the iris. White blood cells (hypopyon) or blood (hyphema) in the anterior chamber will obstruct the view of the iris.
o Irregularities in the shape of the iris should be noted.
o The lens lies posterior to the iris and can appear yellow or opaque if a cataract is present. Patients who have had previous cataract surgery could have a shimmering, reflective quality to their lens.
· Fundus examination
o Most examinations in the office setting do not require dilation. Dilated fundus examinations are performed to assess retinal vascular health or to rule out findings, such as papilledema or vitreous hemorrhage.
o Pharmacologic dilation is usually performed in adults with phenylephrine hydrochloride 2.5% or tropicamide 1%, or both, and causes decreased accommodation for 4 to 6 hours.
o The patient should not be dilated without the direction of an ophthalmologist in the following circumstances: suggestion of a shallow anterior chamber, patient undergoing neurologic observation, and any question of an APD.
OPHTHALMIC SCREENING
· Patients with specific medical conditions or who are taking certain medications should undergo periodic examinations by an ophthalmologist (Table 44-3).
· Other groups of patients should ideally be specifically asked about ocular complaints (Table 44-3).
· The definition of legal blindness in the U.S. is central visual acuity of 20/200 or less in the better eye with the use of a correcting lens. An eye with a visual field that extends <20 degrees is considered to have a visual acuity of <20/200 regardless of the measured acuity.
· Visual requirements for obtaining a driver’s license are determined by each state.
TABLE 44-3 Indications for Ophthalmic Screening
Symptom-Based Approach
VISION LOSS
Acute vision loss should be evaluated immediately in order to rule out processes that have systemic or devastating sequelae, such as giant cell arteritis, acute angle-closure glaucoma, optic neuritis, endophthalmitis, retinal detachment, and posttraumatic processes (ruptured globe, hyphema).
Acute Painless Vision Loss
Is the process transient or is it present for more than 24 hours?
Transient Vision Loss
· Amaurosis fugax
o Etiology: Amaurosis fugax is transient monocular vision loss due to retinal arterial occlusion. The occlusion is usually caused by a cholesterol or platelet embolus but can result from vasospasm. The most common sources of an atheroma resulting in amaurosis fugax are the carotid arteries. Evidence of a Hollenhorst plaque (refractile cholesterol plaque visible in the retinal vasculature) may be seen on physical examination.
o Symptoms: Often described as a shade or curtain coming over the vision that lasts a few minutes, it is most common in patients >50 years or those with a history of vascular disease. A full ophthalmologic examination must be performed by an ophthalmologist to rule out impending vascular occlusion.
o Management: Medical evaluation, including carotid Dopplers, cardiac echocardiography, and basic hematologic workup, should be performed to rule out systemic disease, even in the absence of Hollenhorst plaques. Patients should be sent to an ophthalmologist immediately if the vision loss has not recovered.
· Ophthalmic migraines
o Etiology: A history of migraine may or may not be present. Ophthalmic migraines cause transient episodes that usually lead to at least 5 to 15 minutes of obscuration of vision.
o Symptoms: Fortification (jagged lightning bolts) and scintillating scotomas (blind spot centrally with hazy edges) are characteristic. Colored lights and other visual symptoms can occur. Visual acuity should return to baseline after the episode but headache or mild nausea may follow.
o Management: Careful history should be taken to rule out concomitant neurologic symptoms. Both eyes are usually affected, although it may be sufficiently asymmetric as to appear to be monocular. If truly monocular, then prompt referral to an ophthalmologist is necessary to rule out retinal pathology.
· Pseudotumor cerebri
o Etiology: Pseudotumor cerebri typically occurs in overweight young women and is more common in pregnancy. It is usually idiopathic but may be caused by vitamin A toxicity (>100,000 U/day), cyclosporine, tetracycline, oral contraceptives, or systemic steroid withdrawal.
o Symptoms: Patients will describe headache, transient visual obscurations often associated with changes in posture, diplopia, tinnitus, dizziness, and nausea.
o Management: If disc edema is seen, then a mass or venous thrombosis should be ruled out by an MRI and MR venography. Elevated opening pressure on lumbar puncture with normal cerebrospinal fluid (CSF) composition will confirm the diagnosis. Send patient to an ophthalmologist who can follow visual fields in order to monitor for vision loss and response to therapy. Counsel the patient on weight loss if overweight. Discontinue any causative medications. Medical treatment is achieved with acetazolamide 250 mg PO qid initially, increasing to 500 mg PO qid if tolerated and necessary. Surgery can be considered if medical options fail however this will require input from an ophthalmologist.
Progressive/Stable Vision Loss
· Giant cell arteritis (GCA) or temporal arteritis (ischemic optic neuropathies)
o Symptoms: This potentially life-threatening disease should always be considered when sudden painless vision loss develops in a patient over 50 years old.2,3 Concomitant symptoms of malaise, weight loss, anorexia, scalp tenderness, jaw claudication, or shoulder/limb girdle weakness should be documented.
o Management: Because this is a systemic disease that may lead to bilateral blindness within a few days, early diagnosis and a high level of suspicion are required. Referral emergently to an ophthalmologist is needed to differentiate between causes of sudden painless vision loss that are associated with GCA versus those that have no association or risk of vision loss in the other eye. If there is a high index of suspicion, consider an immediate dose of oral steroids prior to a patient going for blood work (complete blood count [CBC], erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) on their way to the ophthalmologist, or presenting to an emergency room. A temporal artery biopsy should be done within 2 weeks of starting steroids in any patient in whom the clinical suspicion is high.
· Retinal detachment
o Etiology: As the vitreous body pulls away from the retina, it can pull the retina off with it. Patients are at higher risk with increasing age and if they are very near-sighted, postsurgical, or posttrauma. Similar symptoms of acute onset of floaters and occasional flashes but no vision loss may be seen with acute posterior vitreous detachment; however, a dilated exam by an ophthalmologist is still needed to rule out a retinal detachment.
o Symptoms: Presents with constant photopsia (flashing lights), floaters, and sometimes a shade over the part of the vision in one eye. Partial detachments may not affect central visual acuity dramatically, but those that involve the central macular area with significantly decreased visual acuity can be associated with an APD.
o Management: These patients need an emergent extensive dilated retinal examination by an ophthalmologist.
· Vascular occlusions: central retinal artery and vein occlusion (CRAO/CRVO) or branch artery and vein occlusions
o Etiology: This is often seen in people with previously diagnosed vascular disease; it may also occur in younger patients and requires evaluation for embolic (for arterial occlusion) or thrombotic (for venous occlusion) disease. On funduscopic examination, there may be evidence of pallor, vascular box-carring, and a cherry-red spot. Optic nerve swelling, venous engorgement, retinal hemorrhage, and cotton-wool spots, are often collectively described as blood and thunder (CRVO).
o Symptoms: Severe painless vision loss generally to the point of counting-fingers vision or worse. Many will awaken with poor vision or describe the very moment at which the vision was affected. As above, patients must be screened for GCA symptoms if over 50 years old.
o Management: Irreversible damage has been shown to occur after 90 minutes of occlusion and, therefore, patients should be sent to the emergency room or for referral immediately.4
§ If the patient is diagnosed quickly enough with a CRAO, interventional radiologists may be able to treat the patient with catheterization of the ophthalmic artery and injection with thrombolytics, although this is not commonly indicated.5
§ After the acute event, the patient requires a workup for embolic disease and follow-up for late ocular complications including neovascularization and its resultant complications. Follow-up with an ophthalmologist is imperative to treat ocular complications common with these processes.
· Visual field defects
o Etiology: Visual field defects may occur from retinal and optic nerve disease but may also indicate intracranial disease. Lesions anterior to the optic chiasm (e.g., retina, glaucoma, and optic neuritis) produce lesions in one eye only. Pituitary adenomas at the optic chiasm may produce bitemporal field loss. Retrochiasmal (e.g., damage to the optic tracts, radiations, or the occipital cortex) lesions produce homonymous hemianopsias or other homonymous defects. Stroke is the most common cause of homonymous hemianopsia.
o Symptoms: Patients will describe areas in the visual field that are black or missing.
o Management: Generally bilateral visual field loss needs neurologic evaluation and imaging. An ophthalmologist can perform formal visual fields in the office to more precisely determine the pattern of field loss that can help in localization of the pathology.
· Vitreous hemorrhage
o Etiology: Vitreous hemorrhage is often seen in those with diabetes, vein occlusions, and retinal holes or breaks. Vitreous hemorrhage may occur after trauma or with any condition that causes abnormal retinal neovascularization. Terson syndrome is vitreous and retinal hemorrhage in association with subarachnoid hemorrhage (SAH).
o Symptoms: Patients will describe sudden onset of floaters, veils, spider webs, or looking through red (blood). Vision can be moderately or severely impaired depending on the amount of bleeding.
o Management: Have the patient maintain an upright posture with the head of bed elevated while sleeping so that the blood may settle. Refer to an ophthalmologist to monitor progression and treat any retinal pathology. Unresolved hemorrhage may eventually require surgical removal. Stopping anticoagulation should only be considered if there is no risk of systemic complications of discontinuing therapy. Discussion with the ophthalmologist regarding the etiology of the bleed may reveal that discontinuing anticoagulation may be of little therapeutic value.
Acute Painful Vision Loss
· Angle-closure glaucoma
o Etiology: Angle-closure glaucoma is a rare disorder that occurs when the anterior chamber is anatomically narrow and the dilated iris closes off the outflow of aqueous humor causing an acute rise in IOP.6 This event can cause an extremely elevated IOP (possibly up to the 70s), and patients are at risk for vascular occlusions and glaucomatous damage to the optic nerve.
o Symptoms: Severe pain, decreased vision, colored halos, corneal edema, and headache/eye pain. Nausea, vomiting, and abdominal pain may also occur. The pupil is usually fixed and does not react to light.
o Management: Send to an ophthalmologist to manage the IOP initially with medications. But the definitive treatment is a laser peripheral iridotomy, which should be performed as soon as possible; this procedure is also done on the unaffected eye for prophylaxis.6
· Optic neuritis
o Etiology: Optic neuritis is an inflammation of the optic nerve that may involve the optic disc (with hyperemia and optic disc swelling). It may alternatively be retrobulbar (with no apparent optic disc changes but more pain on extraocular motions). Demyelinating disease (multiple sclerosis) is the most common etiology in the proper demographic but is often idiopathic.7,8 Atypical optic neuritis should be worked-up in conjunction with an ophthalmologist/neurologist or neuroophthalmologist.
o Symptoms: Sudden vision loss associated with pain with eye movements and significantly reduced acuity.
o Management: These patients should be followed by an ophthalmologist and referred to a neurologist for imaging to look for demyelinating disease. Autoimmune disease should be investigated should the MRI demonstrate atypical findings or an absence of demyelinating lesions. Treatment consists of either parenteral steroids or supportive care. Oral steroids have not been shown to be effective and may even be deleterious. If the MRI reveals two or more characteristic demyelinating lesions, the patient may benefit from treatment with intravenous (IV) interferon-β within 28 days of symptom onset to decrease the rate of progression to definitive multiple sclerosis.9
Chronic Vision Loss
· Cataract is an opacification of the lens that occurs with aging or secondarily after trauma, chronic inflammation or steroid use, among other causes.
o Etiology: Cataracts are a normal part of aging. They are the most common cause of media opacity and are usually gradual in onset (over months to years). Changes in the lens thickness occur with cataract development and initially can be corrected by a change in glasses.
o Symptoms: As the lens opacifies, patients may note decreased night vision, difficulty with glare, difficulty with reading, and decreased distance acuity. Rarely, patients complain of double vision and decreased color vision and brightness in the affected eye.
o Management: The indication for elective surgical cataract removal is that the cataract affects activities of daily living. Rarely, the cataract may need to be removed if it causes a secondary glaucoma or if it interferes with monitoring other ocular diseases, such as macular degeneration, diabetes, or glaucoma. Elective cataract surgery is performed under local or topical anesthetic as an outpatient and can be offered to any patient who is visually impaired and in stable medical health.
o Anticoagulants required for medical care generally do not need to be discontinued. A recent history and physical examination are required but excessive laboratory testing is not typically indicated.10–13
· Age-related macular degeneration (ARMD) is a disease of the retina that can cause significant visual impairment.
o Etiology: ARMD is a chronic, often progressive disease that affects central vision. It is often bilateral but may be asymmetric. ARMD may be dry (atrophic) or wet (exudative or neovascular). Risk factors include increased age, cigarette smoking, family history, and race (white).14
o Symptoms: Progression is usually slow but sudden profound central vision loss occurs if a subretinal neovascular membrane develops with hemorrhage and scarring.
o Management: Referral to an ophthalmologist to monitor disease is essential. Home monitoring with an Amsler grid is recommended for early detection of central distortion. The Age-Related Eye Disease Study demonstrated that in patients with moderate-to-severe ARMD treatment with vitamins and antioxidants reduced the rate of progression to severe vision loss.15 Injections of anti-VEGF (vascular endothelial growth factor) agents for exudative or wet-type macular degeneration have improved the outcome for this ocular disease.16
· Glaucoma is a neurodegenerative disease that targets the optic nerve. Although glaucoma can be associated with an elevated IOP, this finding is not required for diagnosis.
o Etiology: Glaucoma is a leading cause of blindness in the US. African Americans affected by glaucoma are particularly susceptible to vision loss.17 Patients with a family history of glaucoma should be examined by an ophthalmologist to determine if regular follow-up is indicated.
o Symptoms: Most patients with glaucoma are asymptomatic. Many lose significant peripheral vision before having any visual symptoms. Patients with a history of prior glaucoma surgery are at risk of endophthalmitis. Any patient with prior glaucoma surgery with an acute red eye or pain should be seen immediately by an ophthalmologist.
o Management: These patients need frequent follow-up with an ophthalmologist. Frequency of visits is dictated by the IOP control and the severity of disease. General follow-up is usually every 6 months, with visual field testing every year. Monitoring of optic cup enlargement, especially with concomitant IOP monitoring, is a way to quantify the severity of the progression of glaucoma. Treatment involves medical, laser, or surgical interventions aimed at lowering the IOP.
· Corneal edema
o Etiology: If gradual, it may be due to underlying corneal disease, prior ocular surgery, or trauma. Patients with keratoconus can have acute episodes of corneal edema. Acutely, it may be secondary to increased IOP as in angle-closure glaucoma or rubeosis irides. Inflammation, infection, or opacity of the cornea may be difficult to differentiate from corneal edema with penlight examination.
o Symptoms: Corneal edema is usually associated with pain. There is a hazy appearance of the cornea and decreased vision.
o Management: Referral to an ophthalmologist based on symptom onset and severity.
RED EYE
· Referring to hyperemia or bleeding of the superficial vessels of the conjunctiva, episclera, or sclera, the red eye may or may not be associated with pain.18–20 However, it does not usually cause significantly decreased visual acuity. Contact lens wearers with poor contact lens hygiene presenting with red eye are at high risk for corneal ulcers and should be referred immediately.
· Subconjunctival hemorrhage
o Etiology: A subconjunctival hemorrhage consists of blood over the white sclera and under the clear conjunctiva. The patient should be questioned about other bleeding episodes or bruising, use of anticoagulants and aspirin, and hypertension.
o Symptoms: Although these can be quite dramatic in appearance and alarming to the patient, they are self-limited, do not affect vision, and are generally painless. It may be seen after inadvertent trauma or straining.
o Management: Patients may have mild eye irritation due to increased corneal dryness. Treatment involves cool compresses and artificial tears as needed. If the vision is reduced especially in the setting of trauma, refer to an ophthalmologist. Anticoagulants do not need to be discontinued for an isolated subconjunctival hemorrhage. If multiple episodes occur or if other systemic symptoms are present, a hematologic workup may be indicated.
· Dry eye and blepharitis
o Etiology: Dry eyes are very common, especially in cases of lagophthalmos (incomplete closure) with Bell palsy, thyroid disease, rheumatologic diseases, contact lens wear, and age. Often a decrease in the protein or oil component of the tears due to eyelid disease (rosacea, blepharitis, or meibomianitis) leads to a decrease in the quality, not quantity, of tears. Symptoms of dryness may be worsened by some systemic medications (antihistamines, antidepressants, or hormone replacement). Abnormal contour of the ocular surface can also produce irregularity in the tear film (see pterygium/pinguecula).
o Symptoms: Usually burning, irritation, mildly decreased vision, and foreign body sensation.21 Patients may even complain of overflow tearing with extreme sensitivity to air, light, and prolonged usage of eyes, especially with near vision.
o Management: A trial of artificial tears with carboxymethylcellulose along with eyelid scrubs is often recommended. Referral to an ophthalmologist more acutely if the patient has poor contact lens hygiene (prolonged wear and lack of cleaning) or mechanical cause of dryness (e.g., inability to close the eye due to a seventh nerve palsy).
· Seasonal allergies
o Etiology: Patients with a history of allergies are commonly affected. Frequently, localized allergy to ophthalmic drops can occur and present in a similar fashion. Seasonal allergies are a very common cause of red eyes.
o Symptoms: Itching, redness, tearing, foreign body sensation.
o Management: For occasional use, over-the-counter antihistamines are reasonable, but for chronic use, an ophthalmologist can prescribe more effective medications.
· Injected pterygium and pinguecula
o These are two types of conjunctival degeneration/abnormal growth on the conjunctiva that can become inflamed. They can contribute to corneal dryness as well.
o Treatment is initially with artificial tears, surgical treatment is needed in some cases (see Dry Eye).
· Infections
o Etiology: Infections are a common cause of the red eye. Blepharitis is caused by a mild eyelid infection, which can lead to a foreign body sensation (especially in the morning) and dry eye. Herpes simplex keratitis can lead to corneal ulceration and scarring and should be referred to an ophthalmologist.
o Symptoms: Viral and bacterial conjunctivitis are associated with redness, mucous discharge, crusting, and tearing. In patients with contact lens use and associated redness, prompt referral to an ophthalmologist to rule out corneal ulceration is paramount.
o Management: Although topical antibiotics are useful, topical corticosteroids should not be used without consultation by an ophthalmologist. If symptoms are progressive on treatment or the patient wears contact lenses, prompt referral to an ophthalmologist is necessary.
· Episcleritis and scleritis
o Etiology: Episcleritis is localized inflammation of the episclera. Scleritis is an inflammatory disorder of deeper sclera and can be vision threatening. Scleritis may indicate a serious systemic disease such as a collagen vascular disorder or other autoimmune disease.
o Symptoms: Redness, pain especially to touch. Vision is usually unaffected unless scleritis is posterior or associated with corneal thinning. Episcleral redness blanches with phenylephrine; redness from scleritis does not.
o Management: Patients need to be monitored carefully for the development of scleral thinning and possible perforation. Scleritis is typically treated with systemic steroids; however, evaluation by an ophthalmologist prior to initiating therapy is advised.
· Iritis
o Etiology: Iritis is caused by inflammation of the iris, ciliary body, or both. It can be associated with systemic or localized ocular autoimmune disease. As such, recurrent episodes require a medical evaluation guided by the patient’s history and presentation. This may include CBC, antinuclear antibodies (ANA), rheumatoid factor (RF), syphilis testing, antineutrophil cytoplasmic antibodies (ANCA), human leukocyte antigen-B27, tuberculosis testing, angiotensin-converting enzyme (ACE) level, and/or chest radiography.
o Symptoms: Redness, pain, decreased vision, and light sensitivity. A perilimbal distribution of redness is often present. It can be unilateral or bilateral.
o Management: If suspected, evaluation by an ophthalmologist is indicated.
EYE PAIN
See entries for dry eye, episcleritis/scleritis, corneal abrasion, iritis, angle-closure glaucoma, infections, optic neuritis, corneal edema, and trauma.
OCULAR TRAUMA
· If there is significant (360 degrees) subconjunctival hemorrhage with swelling of the conjunctiva (chemosis), severely decreased vision, eyelid laceration, or a concerning history, referral to an emergency room is warranted to rule out a ruptured globe. An orbital CT with coronal cuts is the preferred study to rule out posterior globe rupture and/or intraocular foreign body. A visual acuity assessment should be attempted by gently lifting even a swollen lid and having a patient read a near-card as this is the “vital sign” of the eye and can guide the physician in triaging the patient.
· If a globe rupture is suspected22
o Keep the eye covered with an eye shield or by taping a disposable cup over it, making sure the rim rests on the bony orbit and not the eye.
o Keep the patient NPO.
o Consider tetanus prophylaxis.
o Administer antiemetics to prevent Valsalva that can expulse the contents of the eye, particularly if the patient must travel a distance to reach the emergency department.
· Chemical burn
o Etiology: Alkaline substances penetrate and saponify tissues and cause severe injury—these include ammonia, sodium hydroxide (lye), calcium hydroxide (lime), magnesium hydroxide, potassium hydroxide, and cement. Acids coagulate the conjunctival surface, and, therefore, penetrate the eye much less. Causative acids include hydrochloric, hydrofluoric, acetic, nitrous, sulfuric, and sulfurous.
o Symptoms: Eye may be red, photophobic, painful, and have epithelial defects detectable with fluorescein and a cobalt blue light/Woods lamp. It may also be white—an ominous sign of complete ischemia.
o Management: Irrigate, irrigate, irrigate! Immediate flushing of the eye with water or normal saline for at least 10 minutes. This can be performed while the patient is transferred to an emergency department.
§ Begin flushing with any neutral fluid that is available.
§ If a Morgan lens is not available, an IV bag connected to nasal cannula placed over the bridge of the nose is effective.
§ Be sure to irrigate the fornices (under the lids) to wash out any particles. Evert the eyelids if necessary.
§ Do not attempt to neutralize the chemical with acidic or basic fluids.
o pH paper should be used to measure the pH of the eye; the pH should be taken a few minutes after the eye has been flushed, before instilling any ophthalmic drops, and it should be 7.0 (if pH paper is not available, the pH square of a urinalysis strip works).
o Rarely, a retained foreign body causes continued release of the chemical and needs to be removed. This is more common with alkali burns.
o Refer to an ophthalmologist when the patient’s condition is stable for evaluation and treatment of chemical damage.
· Corneal abrasion
o Symptoms: Corneal abrasions are common and often present with significant redness, pain, photophobia, or lid swelling after trauma. A topical anesthetic is often used in the office to increase patient comfort. Evaluation can be aided with fluorescein staining and observation with cobalt blue-filtered light. If the history involves grinding metal or projectiles (small or large) refer to an ophthalmologist as there may be a foreign body or a ruptured globe.
o Topical anesthetics aid greatly in examination of the eye but should never be used for treatment, as they may cause epithelial toxicity, decreased healing, and a neurotrophic ulcer.
o Management: Treatment should include antibiotic eye drops (usually sulfacetamide 10%, 1 drop qid for 1 week, or tobramycin 0.3%, 1 drop qid for 1 week) or antibiotic ointment (polymyxin B sulfate [Polysporin Ophthalmic], 1/8-inch strip bid, or erythromycin, 1/8-inch strip bid). If it is certain that the injury has recently occurred (within a few hours), there is no evidence of infection, there is no retained foreign body, and the patient is not a contact lens wearer, the eye may be patched however this is not generally recommended.
o Any corneal haze or evidence of nonhealing abrasion (no improvement in 24 to 36 hours) should be reevaluated by an ophthalmologist.
· Orbital fractures
o Symptoms: Orbital fractures are often seen due to blunt trauma. Patients can be asymptomatic or they can have diplopia at baseline or with extreme gaze. The eyelids are generally swollen—slowly elevate the lid to obtain a visual acuity with a near-card. There may be decreased sensation inferior to the orbit or numbness in the upper teeth on the affected side.
o Management: Referral to an emergency department may be warranted. Orbital CT with axial and coronal cuts is the study of choice. Secondary ocular injuries should be highly suspected when motility is abnormal or vision is markedly decreased. Fractures should be treated with cephalexin 250 mg PO qid for 10 days. Emphasis on no nose blowing and oxymetazoline tid for 3 days aids in decreasing the risk of extension of sinus disease into the orbit and limits orbital emphysema. While many fractures need no surgical repair, referral to a surgeon should be expedited should there be diplopia in primary gaze and/or significant enophthalmos (recession of the eyeball into the orbit).
· Foreign body/rust ring
o Symptoms: pain, redness, decreased vision with a history of working around grinding metal, a dirty environment, or other environmental factors that can lead to small particles becoming lodged in the anterior surface of the eye.
o Management: Foreign bodies can be carefully removed with either a wet cotton tip or needle under direct visualization using a slit lamp. A burr drill is occasionally used to remove rust rings. After the foreign body is removed, the eye should be treated with topical antibiotic (see the “Corneal Abrasions” section). Eversion of the eyelid should be performed to rule out retained foreign bodies under the eyelid. Generally, the patient should be referred to an ophthalmologist.
· Traumatic iritis and hyphema
o Etiology: Traumatic iritis must be differentiated from bleeding (microhyphema) and infection. Hyphema is blood in the anterior eye chamber and may lead to decreased vision, photophobia, and a dull achiness around the eye. Usually, it is a result of direct trauma to the eye, but it can be caused by abnormal blood vessels (secondary to tumors, diabetes, chronic inflammation, intraocular surgery, etc.).
o Symptoms: Traumatic iritis is common 2 to 3 days after blunt trauma and may present with decreased vision, photophobia, and dull pain. A hyphema presents more acutely posttrauma with decreased vision; however, both need to be seen and treated by an ophthalmologist.
o Management: Pain and decreased vision after trauma should be evaluated and followed by an ophthalmologist to rule out additional ocular involvement and manage possible complications such as rebleeding in the eye, increased IOP, and corneal blood staining. Hyphema is often treated with dilation, light activity, rigid shield, and topical steroid medication, but may require surgical washout if medical management is insufficient. The status of sickle cell disease/trait should be noted, as it affects the clearance of red blood cells from the anterior chamber through the trabecular meshwork and may lead to complications.
DOUBLE VISION
· Monocular diplopia is refractive in nature and should be evaluated by an ophthalmologist usually on a routine basis unless in the setting of trauma.
· Binocular diplopia has a larger differential.23,24 Asking if the double vision resolves by closing either eye is a good way to differentiate monocular versus binocular diplopia. If the patient notes resolution of diplopia after covering either eye, then it is likely binocular diplopia. The essential job of the clinician is to examine the patient’s eye movements and evaluate the cranial nerves (CN).
· Abnormal motility
o Abnormalities of eye motility may suggest an acute or chronic CN palsy (III, IV, or VI) or extraocular muscle disorder.
o Acute abnormalities are usually accompanied by complaints of diplopia, which may be horizontal or vertical in nature.
o Chronic motility defects may be asymptomatic.
o Medical conditions such as thyroid eye disease (especially Graves disease), idiopathic inflammatory pseudotumor (ocular myositis), myasthenia gravis (MG), giant cell arteritis, demyelinating disease (multiple sclerosis), and cerebellar dysfunction may manifest with abnormal eye movements.
· Ocular myasthenia gravis
o Etiology: MG is an autoimmune-mediated disease or rarely myasthenia-like from medications like penicillamine or aminoglycosides. Patients may have an associated thymoma or Graves disease.
o Symptoms: Drooping of eyelids worse at the end of the day or with fatigue, intermittent binocular double vision especially if worse with fatigue.25 Additional symptoms include difficulty swallowing, breathing, and proximal limb weakness.
o Management: By far the most common cause of ptosis is levator dehiscence; however, MG should always be included in the differential. In the office, one can have the patient look up at your finger for 1 minute to assess fatigability of the ptosis. If it worsens with prolonged up-gaze, one should entertain the possibility of MG. It may then be prudent to refer the patient to a neurologist for more testing while ordering MG antibodies (anti-ACHr, anti-MuSK, striational/titan antibodies) and thyroid function tests (including thyroid-stimulating antibody [TSI]).
· Thyroid disease/Graves disease
o Etiology: The most common cause of unilateral AND bilateral proptosis is thyroid eye disease. Graves disease is an autoimmune disease associated with hyperthyroidism. However, thyroid eye disease may appear or progress in patients who are clinically euthyroid or hypothyroid. Tobacco usage has been associated with higher incidence of ocular complications.
o Symptoms: The most common manifestations include eyelid retraction, double vision, proptosis, and corneal dryness.
o Management: Referral to an ophthalmologist with an orbital CT with axial and coronal cuts in conjunction with thyroid testing (thyroid stimulating hormone [TSH], free thyroxine [T4], TSI) is critical. Smoking cessation is essential for managing these patients.
· Intracranial aneurysm
o Rarely intracranial aneurysms may present with ocular CN defects.
o Involvement of CN III–VI should suggest cavernous sinus pathology.
o Pupil-involving CN III defects can be seen in posterior communicating artery aneurysms, and MR angiography may be helpful in diagnosis.
o Diabetic or microvascular ischemic third nerve palsy usually spares the pupil and recovers spontaneously.
EYELID DISORDERS
· These problems can overlap with the red eye entities. For example, eyelid crusting, especially in the mornings with foreign body sensation and mild blurred vision especially in a patient with acne rosacea is most like blepharitis-associated dry eye.
· Keep in mind that malignant eyelid lesions include basal cell, squamous cell, and sebaceous cell carcinomas, and can mask as chronic eyelid disease.26
· Chalazion/hordeolum
o Etiology: A chalazion is a chronic lipogranulomatous inflammatory lesion due to an obstructed meibomian gland in the eyelid. A hordeolum, or stye, is an acute, painful inflammatory lesion of eyelid glands, and is typically caused by a staphylococcal infection.
o Symptoms: Each may initially present with acute inflammatory signs while a chalazion develops into a relatively painless nodule, a hordeolum can incite a localized cellulitis.
o Management: Mainstays of treatment are hot compresses with gentle massage along with topical or oral antibiotics if indicated. If the lesion has not completely resolved and is no longer actively inflamed, surgical incision and drainage may be recommended. Rarely, a chalazion may be mistaken for a malignant lesion and vice versa so referral to an ophthalmologist is warranted especially if the lesion does not resolve in 4 weeks.
· Cellulitis
o Etiology: Preseptal cellulitis is usually secondary to localized trauma or skin defect (scratch, cut, rash) while orbital cellulitis is secondary to sinus disease in an overwhelming majority of cases.
o Symptoms: Swelling of the eyelids with pain, warmth, and tenderness to touch without motility or visual disturbances is preseptal. If there is difficulty with eye motility or decreased vision then the process affects the postseptalorbit and can threaten the globe or cavernous sinus.
o Management: Preseptal cellulitis can be managed conservatively with oral antibiotics (amoxicillin/clavulanate 875/125 mg PO bid for adults or trimethoprim/sulfamethoxazole 160/800 mg, one tablet tid to two tablets bid in those allergic to penicillin). Worsening preseptal cellulitis while on oral antibiotics or orbital cellulitis needs admission for IV antibiotics along with an orbital CT scan. Rarely orbital inflammatory disease can manifest as orbital cellulitis especially if there is no sinus disease on orbital CT scans. Consultation by an oculoplastic surgeon in these cases is advised.
· Herpes zoster ophthalmicus (HZO)
o Etiology: Varicella-zoster virus.
o Symptoms: Dermatomal skin rash with pain, paresthesias, and vesicles (later in the disease). Sometimes eye redness, decreased vision, and eye pain occur. Hutchinson sign (rash on the tip of the nose) is associated with intraocular involvement. HZO is almost always unilateral and does not cross the midline.
o Management: If <40 years old, consider testing for HIV. Oral acyclovir 800 mg PO 5×/day or valacyclovir 1,000 mg tid for 7 to 10 days when the patient presents within the first week of symptoms. Erythromycin ointment to skin lesions. If there is any eye pain, referral to an ophthalmologist within a few days is advised. If there are signs of motility abnormalities, an APD, or concern for orbital involvement, then admission for IV acyclovir should be initiated.
· Ptosis and dermatochalasis
o Etiology: Ptosis is a common condition that may occur from congenital disease, neurologic disease, or involutional changes with aging. Dermatochalasis is excess eyelid skin that may cause symptoms similar to those of ptosis.
o Symptoms: Eyelid drooping or excess skin obstructing the vision. See the section on Myasthenia Gravis above.
o Management: If the upper eyelid appears to interfere with the superior field of vision, or if the patient is symptomatic, surgical intervention is possible. Blepharoplasty is the treatment for symptomatic dermatochalasis. If there is any suspicion of a mass occupying the orbit or neurologic disease (both of which can present with eyelid droop), referral to an ophthalmologist can aid in the diagnostic evaluation.
· Dacryocystitis
o Etiology: Dacryocystitis is an infection of the tear sac from inadequate drainage of tear.
o Symptoms: Dacryocystitis presents with redness, pain, and swelling in the inferomedial part of the lower eyelid.
o Management: Acutely, oral antibiotics are necessary (cephalexin, 250 mg PO qid for 10 days). Surgical dacryocystorhinostomy is usually required after the inflammation has resolved because recurrences are likely. An ophthalmologist or oculoplastic surgeon can aid in the management of this condition as other entities including chalazion/hordeolum, canaliculitis, and lacrimal sac tumors can have similar presentations.
REFERENCES
1.Payne JW, Duke JR, Butner R, et al. Basal cell carcinoma of the eyelids. A long-term follow-up study. Arch Ophthalmol 1969;81:553–558.
2.Weyand CM, Goronzy JJ. Giant-cell arteritis and polymyalgia rheumatica. Ann Intern Med 2003;139:505–515.
3.Waldman CW, Waldman SD, Waldman RA. Giant cell arteritis. Med Clin North Am 2013;97:329–335.
4.Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723–736.
5.Schumacher M, Schmidt D, Jurklies B, et al. Central retinal artery occlusion: local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010;117:1367–1375.
6.Lam DSC, Tham CCY, Lai JSM, et al. Current approaches to the management of acute primary angle closure. Curr Opin Ophthalmol 2007;18:146–151.
7.Balcer LJ. Clinical practice. Optic neuritis. N Engl J Med 2006;354:1273–80.
8.Chen L, Gordon LK. Ocular manifestations of multiple sclerosis. Curr Opin Ophthalmol 2005;16:315–320.
9.CHAMPS Study Group. Interferon beta-1a for optic neuritis patients at high risk for multiple sclerosis. Am J Ophthalmol 2001;132:463–471.
10.Cavallini GM, Saccarola P, D’Amico R, et al. Impact of preoperative testing on ophthalmologic and systemic outcomes in cataract surgery. Eur J Ophthalmol 2004;14: 369–374.
11.Keay L, Lindsley K, Tielsch J, et al. Routine preoperative medical testing for cataract surgery. Cochrane Database Syst Rev 2012;(3):CD007293.
12.Schein O, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract surgery. Study of Medical Testing for Cataract Surgery. N Engl J Med 2000;342:168–175.
13.Guirguis-Blake J. Preoperative testing for patients undergoing cataract surgery. Am Fam Physician 2009;80:1228.
14.de Jong PT. Age-related macular degeneration. N Engl J Med 2006;355:1474–1485.
15.Chew EY, Clemons TE, Agrón E, et al. Long-term effects of vitamins C and E, β-carotene, and zinc on age-related macular degeneration: AREDS report no. 35. Ophthalmology 2013;120:1604–1611.
16.Cheung CMG, Wong TY. Treatment of age-related macular degeneration. Lancet 2013;382:1230–1232.
17.Bourne R, Price H, Stevens G; GBD Vision Loss Expert Group. Global burden of visual impairment and blindness. Arch Ophthalmol 2012;130:645–647.
18.Cronau H, Kankanala RR, Mauger T. Diagnosis and management of red eye in primary care. Am Fam Physician 2010;81:137–144.
19.Wirbelauer C. Management of the red eye for the primary care physician. Am J Med 2006;119:302–306.
20.Leibowitz HM. The red eye. N Engl J Med 2000;343:345–351.
21.Bernardes TF, Bonfioli AA. Blepharitis. Semin Ophthalmol 2010;25:79–83.
22.Romaniuk VM. Ocular trauma and other catastrophes. Emerg Med Clin North Am 2013;31:399–411.
23.Friedman DI. Pearls: diplopia. Semin Neurol 2010;30:54–65.
24.Rucker JC, Tomsak RL. Binocular diplopia. A practical approach. Neurologist 2005;11:98–110.
25.Vaphiades MS, Bhatti MT, Lesser RL. Ocular myasthenia gravis. Curr Opin Ophthalmol 2012;23:537–542.
26.Zucker JL. The eyelids: some common disorders seen in everyday practice. Geriatrics 2009;64:14–19, 28.