Ocular Emergencies in Primary Care: Diagnosis, Treatment, and Referral
Neil Patel, MD; Gonzalo Ortiz, MS; Norberto Mancera, MD; and Hershel Patel, MD
Patel N, Ortiz G, Mancera N, Patel H. Ocular emergencies in primary care: diagnosis, treatment, and referral. Consultant. 2016;56(10):892-896.
ABSTRACT: Primary care providers must quickly diagnose, make referrals, and initiate treatment for a variety of ocular conditions and diseases. Delays in treatment during an ocular emergency can result in permanent vision loss, and thus a broad knowledge of the most vision-threatening pathologies is vital. This article reviews the definitions, etiology, presentations, and treatment for retinal detachment, acute angle-closure glaucoma, amaurosis fugax, and corneal ulcer.
KEYWORDS: Glaucoma, angle closure glaucoma, retinal detachment, amaurosis fugax, transient visual loss, corneal ulcer, keratitis
As the initial point of contact for patients, primary care physicians must quickly diagnose, make referrals, and initiate treatment for a variety of ocular conditions and diseases. Delays in treatment during an ocular emergency can result in permanent vision loss, and thus a broad knowledge of the most vision-threatening pathologies is vital. This article reviews the definitions, etiology, presentations, and treatment for the following 4 ocular emergencies: retinal detachment (RD), acute angle-closure glaucoma (AACG), amaurosis fugax (AF), and corneal ulcer.
RD is a condition in which the neurosensory retina has separated from the underlying retinal pigment epithelium (RPE), resulting in vision loss (Figures 1 and 2).
Figure 1. The retina temporal to the optic disc is detached and bullously elevated. The detachment extends shallowly into the macular area. (Photo courtesy of Leonid Skorin Jr, DO)
Figure 2. The image focus is on the detached retina. The whitish-yellow appearance represents loss of the underlying choroidal red reflex. (Photo courtesy of Leonid Skorin Jr, DO)
There are 3 types of RD: rhegmatogenous RD (RRD), tractional RD (TRD), and exudative RD.1
RRD occurs when a tear in the retina allows for vitreous fluid to flow into and separate the sensory retina from the RPE. As the most common form of RD, it has a reported annual incidence rate between 6.3 and 17.9 cases per 100,000 population and occurs bilaterally in approximately 7.26% of cases.2 A history of myopia (nearsightedness), cataract surgery, or trauma in an elderly symptomatic patient should alert the clinician to consider a diagnosis of RRD. Myopia results in a 4-fold increase of RD in eyes with a refractive error of −1 to −3 compared with nonmyopic eyes.3 Prior to improvements in cataract surgery and the adoption of phacoemulsification, a history of cataract surgery resulted in an estimated 5.5 times higher probability of RD; this number has since decreased.4 The incidence of RD following phacoemulsification had been 0.25% from 1999 to 2001 and has continued to decline over time.5
TRD has an insidious onset and occurs when adhesions develop between the vitreous gel and the retina. The fibrotic adhesive tissue forms as a result of previous hemorrhage, injury, surgery, infection, or inflammation and allows mechanical forces to separate the retina from the RPE without causing a retinal tear or break.
Exudative RD occurs when subretinal fluid accumulates and causes separation without a retinal break. This is usually caused by hydrostatic factors, tumor growth, or inflammation; treatment is geared toward the underlying etiology, with a relatively better visual prognosis.6
Non-RRD has a subacute/chronic visual loss progression and is therefore not considered as emergent as RRD.
As a person ages, the vitreous gel liquefies and shrinks, resulting in traction forces on the retina, which can cause posterior vitreous detachments (PVD) that can result in a retinal tear and lead to RRD.6 Retinal tears present as acute-onset floaters and/or flashes, with hemorrhage detected via slit-lamp examination highly indicating a retinal tear. Patients who initially receive a diagnosis of uncomplicated PVD (ie, development of floater without hemorrhage) have a 3.4% chance of a retinal tear within 6 weeks7; thus, it is vital for these patients’ cases to be followed by an ophthalmologist.
Initial symptoms of RD include photopsia (the sensation of flashing lights), often accompanied by floaters, and unlike the symptoms of a PVD, vision loss. Over time, the patient may report seeing a shadow in the peripheral visual field. If the macula is involved, the patient will experience a severe loss in visual field and visual acuity. Patients with suspected RD should be advised to avoid putting any pressure on the globe and to limit any activity until further assessment. The ocular examination of these patients should include assessment of near visual acuity and distance acuity, confrontation visual field examination, pupillary reaction assessment, intraocular pressure measurement, slit-lamp examination, and dilated fundus examination. Indirect ophthalmoscopy with scleral depression can be used for the definitive diagnosis of RD, which appears as a gray area with dark blood vessels on retinal examination. Additionally, B-scan ultrasonography can be used if media opacities are present.1
Visual acuity at presentation helps determine prognosis and guide treatment. The better a patient’s preoperative visual acuity, the higher likelihood they will retain the same level of vision postoperatively. Prompt diagnosis of RD is crucial, because immediate surgery can improve visual outcomes in patients who initially have a macula-sparing RD; once the macula is involved, the potential to preserve vision is drastically reduced. Thus, every effort should be made to promptly refer a patient to a retinal surgeon if RD is suspected.6 Postoperatively, 80% of patients with macula-sparing RD achieve 20/50 acuity or better. If macular detachment is present and surgery occurs within 7 days, approximately 60% of patients will regain 20/50 or better vision, 35% will have 20/60, and 5% will have less than 20/400.8
Treatment of RRD and TRD is primarily surgical. If the patient is asymptomatic, a retinal hole or tear without evidence of detachment can be treated by laser photocoagulation or cryoretinopexy to prevent RD. This results in scar formation around the tear that helps anchor the retina and prevents unwanted fluid accumulation. Larger or symptomatic RDs are generally treated with pneumatic retinopexy (PR), scleral buckle (SB), or vitrectomy.
PR is a nonincisional alternative to SB that consists of injecting an expanding gas bubble to seal the RD, whereas SB is a band that encircles the eye, is placed underneath the conjunctiva to approximate the detached retina, and allows for reattachment. The gas bubble in PR is removed, whereas the band in SB is often left in place indefinitely. Patients should be made aware that air travel is an absolute contraindication in PR. The decision about which procedure to pursue should be made by a specialist given that proper case selection is critical to achieving favorable results.9
Acute Angle-Closure Glaucoma
Glaucoma is classically defined as an optic neuropathy and refers to a group of eye diseases that are typically associated with an increase in intraocular pressure (IOP). Primary angle-closure glaucoma (PACG) is a subset of glaucoma caused by the narrowing or closing of the anterior chamber angle. This causes inadequate drainage of the aqueous humor and a subsequent elevation in IOP that leads to optic nerve damage. PACG is present in only 26% of patients with glaucoma but is responsible for half the cases of glaucoma-related blindness.10
An acute occlusion of the angle is referred to as AACG and must be immediately recognized and treated.
Many anatomic abnormalities can increase the risk of developing AACG, including a narrow angle, shallow anterior chamber, thin iris, thin ciliary body, and short axial eye length. Other risk factors include female sex, hyperopia, age greater than 60 years, and Inuit or Asian ethnicity.11,12 Clinicians should be aware that the following medications have been known to cause AACG: local or systemic adrenergic agents, drugs with anticholinergic effects, tricyclic and tetracyclic antidepressants, and cholinergic agents such as pilocarpine. Of note, sulfa-based drugs such as topiramate can cause AACG by ciliary body edema with anterior rotation of the iris-lens diaphragm, for which iridotomy (a commonly employed laser surgery) is not effective.13
Patients present with severe ocular pain, decreased vision, nausea and vomiting, intermittent blurring of vision with halos, and headache. Symptoms occur more often in the evening, since dimmer light causes mydriasis. Physical examination can show conjunctival injection, corneal edema/cloudiness, a mid-dilated pupil (4-6 mm) that does not react well to light, or decreased vision. These patients can also have pain on eye movement and a firm globe. IOP should be quickly measured in these patients and usually ranges from 40 to 90 mm Hg. If the pressure is greater than 20 mm Hg in the context of these findings, the diagnosis of AACG is likely. Confirmatory diagnosis relies on gonioscopy and may be aided by anterior segment optical coherence tomography or ultrasonography.14
Once AACG is suspected, treatment is designed to immediately control IOP while monitoring changes to the angle and optic nerve head.10 These patients should stay in the supine position and should not place any covering over the affected eye (to prevent mydriasis). While medical and surgical treatment is being prepared, corneal indentation can be started with repeated indentation of the central cornea with a gonioscopy lens for 30 seconds, followed by a 30-second rest, over 10 to 15 minutes, which may mechanically open the angle. Medical management includes oral acetazolamide and topical timolol, pilocarpine, and apraclonidine.
Pilocarpine a cholinergic agent, is used to induce miosis, whereas acetazolamide, a carbonic anhydrase inhibitor, and the β-blocker timolol, work by decreasing the rate of aqueous humor production. The α-adrenergic agonist apraclonidine has a minor α1 mydriatic effect but actually lowers IOP by decreasing aqueous production. Hyperosmotic agents such as oral glycerin or intravenous mannitol are the most effective medical means of lowering IOP during an attack but should be used with caution due to their possible systemic complications from volume redistribution. A topical corticosteroid such as prednisolone, 1%, is given to decrease inflammation. Because nausea and vomiting can increase IOP, antiemetics should also be given.
An ophthalmologist should be consulted for laser and surgical considerations. Laser procedures such as peripheral iridotomy and peripheral iridoplasty can be helpful when the patient is not responding to medical therapy. An iridotomy creates a hole in the iris, whereas an iridoplasty causes circumferential scarring of the iris, causing it to contract or flatten and pull away from the closed angle. Both procedures help increase aqueous humor flow.14,15
Alternatively referred to as transient visual loss (TVL), AF is considered equivalent to a transient ischemic attack and often signifies an impending stroke or retinal vessel obstruction. The causes of AF can be divided into 5 possible etiologies: embolic, hemodynamic, ocular, neurologic, and idiopathic. Overall, AF is commonly caused by carotid artery disease leading to emboli or vascular insufficiency. A prospective study of 337 patients with TVL found that 10% of patients had an ipsilateral internal carotid artery (ICA) stenosis between 1% and 69%, 30% of patients had an ipsilateral ICA stenosis of 70% to 99%, and 13% of patients had an ipsilateral ICA occlusion.16 Of note, carotid emboli into the ophthalmic circulation is an important marker of generalized atherosclerotic disease.
Other carotid pathologies include fibromuscular dysplasia, dissection, and aneurysm. A change in posture, exercise, or exposure to bright light can trigger retinal vascular insufficiency if extracranial arterial occlusive disease is present. Neurologic causes include intraorbital masses, brain tumors, multiple sclerosis, and migraines. Rare causes include narrow-angle glaucoma, intraocular hemorrhage, congenital anomaly of the optic disc, disc drusen, and orbital tumor.17
The patient may report painless transient monocular vision loss, starting in the upper fields and progressing inferiorly. Episodes usually have an abrupt onset and last seconds to minutes, leaving no permanent visual deficits. Rarely, vision loss can be binocular and last for several hours, in which case vertebrobasilar insufficiency should be considered. Despite a patient’s return to baseline vision, a complete ocular examination, including a dilated retinal evaluation, should be done by an ophthalmologist, looking for emboli, optic disc swelling, and retinal whitening. Often, no evident precipitating signs or factors are identified, and examination findings may be normal.
Bright yellow lesions within retinal vessels are indicative of cholesterol emboli called Hollenhorst plaques and are the most common emboli occurring in the eye. Persistence of visual loss indicates a more serious retinal or optic nerve infarction.1,18
Pressing laboratory tests should include an erythrocyte sedimentation rate to rule out giant cell arteritis, which can present as TVL and rapidly lead to permanent vision loss. Additionally, a complete blood cell count and platelet count looking for evidence of a hypercoagulable state is important. Carotid imaging followed by a full cardiac evaluation in patients with AF is justified, given the increased frequency of cardiac mortality in patients who experience AF. Additionally, a lipid panel and hemoglobin A1c assessment are warranted to screen for hyperlipidemia and diabetes mellitus, respectively.
The management of AF is dictated by the underlying etiology; thus, a proper diagnosis is vital.
Observation is an option in patients whose laboratory test findings and imaging results are normal. Management of risk factors for carotid and cardiac disease such as hypertension and diabetes is critical, as are lifestyle modifications such as smoking cessation.
For patients with atherosclerotic disease, aspirin is the mainstay of treatment, and carotid endarterectomy can be considered in symptomatic patients with severely stenosed carotid arteries. Follow-up with a patients’ primary care provider is crucial to preventing further episodes or complications.18
A corneal ulcer is defined as a defect in the epithelial layer of the cornea with involvement of the deeper stroma, usually caused by infection. Corneal ulcers commonly have bacterial etiologies, although viral and fungal etiologies also occur. Viral keratitis typically occurs on a previously intact epithelium, while bacterial keratitis can occur after a traumatic break in the corneal epithelium that creates an entry point for bacteria. Common causes of corneal trauma are abrasions from ocular foreign bodies, improper contact lens hygiene, malnutrition, and tear insufficiency. Besides inappropriate contact lens wear/hygiene and trauma, ocular surface disease and prior ocular surgery are also risk factors for corneal ulcer.
Common bacterial organisms in cases of corneal ulcer include Pseudomonas aeruginosa, coagulase-negative staphylococci, Staphylococcus aureus, Streptococcus pneumoniae, and Enterobacteriaceae. Viral keratitis is typically caused by herpes simplex virus (HSV) and varicella-zoster virus (VZV). Common causes of fungal keratitis include Fusarium and Aspergillus species, and Acanthamoeba, a protozoan that also causes keratitis in a small number of patients.19,20
Patients with a corneal ulcer will typically present with eye pain, erythema of the eyelid and conjunctiva, foreign body sensation, and in some cases, blurred vision and light sensitivity. It is important to ask these patients about their contact lens use, including whether they use hard or soft contacts, the type of contact lens solution they use, and contact lens hygiene.21 These patients should be asked about ocular medications, especially corticosteroids, previous eye surgery or ocular disease, and other comorbidities such as diabetes mellitus, immunodeficiency diseases (eg, HIV), and autoimmune diseases (eg, rheumatoid arthritis), since these can cause noninfectious keratitis.
A thorough eye examination is needed, including visual acuity assessment, slit-lamp examination, and IOP measurement. The eye will typically look erythematous with a white corneal lesion indicating stromal infiltration. Based on the location of the lesion, vision might be obstructed. The size, shape, and borders of the ulcer should be noted to help with follow-up and diagnosis. Fluorescein staining helps to better visualize the epithelial defect if it is not easily evident. All ulcers should be cultured, and sensitivities ordered, since determining the infectious etiology is necessary to guide treatment.20
HSV keratitis is the most common cause of viral ulcer in the United States, and it classically presents as a branching dendritic ulcer. VZV keratitis can be seen in shingles infection involving the ophthalmic branch of the trigeminal nerve. Loss of corneal sensation is commonly seen in VZV keratitis compared with HSV infection, and the classic dendritic pattern is not seen in VZV.22 Bacterial keratitis is commonly associated with mucopurulent discharge from the eye, with P aeruginosa characteristically causing a bluish green discharge.1
Immediate initiation of a topical antibiotic followed by prompt referral to an ophthalmologist is imperative to prevent further ulcer progression. Most bacterial ulcers are treated with a third- or fourth-generation fluoroquinolone (ophthalmic) every 30 to 60 minutes if the lesion is small and noncentral in the cornea.
Culturing and fortified antibiotics such as tobramycin and a cephalosporin or vancomycin instituted by an ophthalmologist are appropriate for severe, deep, or central corneal ulcers. When culture and sensitivities results return, antibiotic therapy can be further targeted.23
If the patient presents with discomfort due to ciliary muscle spasms, cycloplegics such as scopolamine can be used to induce mydriasis. If the ulcer is found to be viral, then antiviral treatment should be initiated. An ophthalmologist should closely follow the patient’s case until resolution of the corneal ulcer.20
Neil Patel, MD, is a recent graduate of the Morsani College of Medicine at the University of South Florida in Tampa and is an internal medicine intern at Louisiana State University in Shreveport.
Gonzalo Ortiz, MS, is a fourth-year student at the Morsani College of Medicine at the University of South Florida in Tampa.
Norberto Mancera, MD, is an ophthalmology resident at the USF Eye Institute in Tampa, Florida.
Hershel Patel, MD, is a second-year ophthalmology resident at the USF Eye Institute in Tampa, Florida.
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