Authors:David D. Markoff, MD, FACS,Mountain Eye Associates, Centro Médico Regional Haywood, Clyde, NC; undDavid Chacko, MD, PhD,Associate Professor, Department of Ophthalmology, University of Nebraska Medical Center, Omaha, NE.
Reviewers:Donald J. Keller, MD,Clinical Professor, University of Colorado, Boulder; YDr. John Peters,Clinical Professor of Ophthalmology, Creighton University, Omaha, NE; Clinical Professor, University of Nebraska Medical Center, Omaha.
Representations of eye-threatening problems can be subtle or dramatic. Pain may or may not be present. Vision loss is not always a major initial complaint, although subsequent vision testing may reveal significant field or perceptual deficits. But regardless of first impressions, the clinical and medicolegal consequences of a poorly managed eye emergency can be devastating. Consequently, the patient's assessment must always be systematically, accurately, and carefully documented.
The fact is that, perhaps more than many other conditions, eye-related emergencies require accurate diagnosis, thorough evaluation, and targeted treatment to optimize clinical outcomes. In addition, the spectrum of ocular and retinal pathologies that require emergency treatment is wide, and most patients with unusual conditions or acute blindness require an ophthalmological consultation as part of their treatment plan.
"Pink eye" is one of the most common symptoms that prompts a visit to the emergency department to evaluate an ophthalmic problem. Some causes are relatively benign (allergic reactions, subconjunctival hemorrhage, bacterial conjunctivitis), while other etiologies, such as angle-closure glaucoma or endophthalmitis, can be vision-threatening and require urgent treatment, including vision-sparing surgery.
In addition to requiring a complete physical examination with a slit lamp, ocular trauma may require additional modalities, such as plain radiographs or CT scans, to detect orbital penetration and delineate the location of an intraorbital foreign body. It is important to assess the probability of orbital rupture in cases of blunt trauma to the eyeball. Trauma/chemical burns of the globe require toxin-specific treatment with targeted therapy, depending on the nature of the causative agent. Prompt eyewash is a mainstay of treatment for these injuries.
Decoding the cause of non-traumatic vision loss is an essential part of managing ophthalmic emergencies. The most common causes are optic nerve dysfunction, retinal pathology, or retinal vascular occlusion, all of which can be suspected at first sight and require immediate treatment to preserve vision. Diplopia, another common presentation, may indicate an acute neurologic deficit that may be vascular (ie, a third CN palsy induced by a posterior communicating artery aneurysm) or degenerative (multiple sclerosis) in etiology.
The purpose of this article is to provide a concise and focused overview of common eye emergencies that are treated in the ER. By emphasizing those conditions that require immediate treatment to save sight, this review describes a systematic approach to ophthalmic evaluation, presents testing guidelines, indications for referral, and effective treatment pathways for outcomes.
- The editor
The eye exam can be divided into the eight parts listed in Table 1.
|Table 1. The eye exam|
|• visual acuity|
|• External eyelids, eyelashes, lacrimal glands, periorbital|
|• Extraocular mobility|
|• Fields of vision|
|• Intraocular pressure|
For medical and legal reasons, visual acuity must be checked in all patients with eye problems. This is usually done for distance vision using a standard visual acuity (Snellen) chart and is recorded first for the right eye and then for the left eye. A nearby map can also be used and is particularly useful for bedridden patients. Visual acuity can be checked with and without correction, and the most important information is usually the "best corrected" visual acuity. If the patient has not brought or does not have glasses, a pinhole occluder can provide a good approximation of corrected visual acuity.
External examination should look for signs of trauma, eyelid disease, proptosis, etc.
Examination of the pupils is important, especially in patients with significant vision loss. The swinging lantern test is used to check for a relative afferent pupillary defect.1
Extra-ocular movements (EOMs) are checked by having the patient follow an object while keeping the head still. Pay special attention to signs of paralysis or muscle deterioration. Postpone MOE testing if an open globe injury is suspected.
A confrontational visual field is performed by presenting two objects (usually both hands of the examiner) separately in front of each eye and asking the patient to indicate whether they can count the fingers on each hand. This is particularly useful for detecting hemianopic field defects.
Biomicroscopy of the anterior segment of the eye is best performed with a slit lamp. A direct ophthalmoscope with the +10 lens inserted also works well. Pay particular attention to abnormalities of the cornea, anterior chamber (eg, hyphema), and iris.
Intraocular pressure is tested unless an open eyeball is suspected. A Goldmann-type applanation tonometer is most suitable. The portable Tonopen (mentor) also works well in an emergency.
Fundus examination is best performed with dilated pupils (use 1% tropicamide and 2.5% phenylephrine). Carefully document all dilating drops administered to patients with traumatic brain injury.2A direct ophthalmoscope provides a good view of the optic nerve, macula, and vessels. Indirect ophthalmoscopy is required for examination of the peripheral retina.
A red eye may indicate a vision-threatening process or a self-limiting benign condition. Examination findings that help separate the different etiologies are listed in Table 2.
|Table 2. Red eye results.|
Clear or watery discharge with allergic processes, superficial abrasions and viral infections. Yellowish or purulent discharge more common in bacterial conjunctivitis.
Seen in most viral infections, including herpes simplex. Gonococcus only bacterial conjunctivitis with a preauricular node.
Fibrinous membranes over the eyelids are more common with adenoviral or herpetic viral infections, streptococcal or gonococcal bacterial infections, and chemical burns._______________________________________________________________
Common non-traumatic causes of red eye and recommended treatments are listed below. (Traumatic causes are given in a later section.)
hyposphagmaUsually spontaneous onset without pain or decreased vision. Examination reveals a solid bright red patch on the bulbar conjunctiva with well-defined borders. If the patient has a history of trauma, look for other injuries. Treat by observation. Coagulation parameters should be checked if there are multiple recurrences or other signs of excessive bleeding.3
Allergic reaction.The patient has symptoms of itching, burning and tearing. There is often a history of systemic allergic problems. Examination shows injected conjunctiva, possible chemosis, and watery discharge. Treatment with cold compresses, elimination of the causing allergen and medication if necessary. Naphazoline and others are available without a prescription. Histamine blockers, such as levocarbastine, help with acute symptoms. Mast cell inhibitors (lodoxamide tromethamine, cromolyn) help prevent future attacks. Olopatadine hydrochloride combines histamine blockade and mast cell inhibition.
Viral infections (not herpetic).Patients often have a history of exposure to conjunctivitis or a concurrent upper respiratory tract infection. Examination shows preauricular adenopathy, watery discharge, possible conjunctival membrane. The cornea may show grayish round subepithelial lesions. The patient may have eyelid edema, especially with adenovirus. Treatment for most viral conjunctivitis consists of cold compresses and observation (adenovirus infections can take 2-3 weeks to clear up and are highly contagious). As a prophylaxis against secondary bacterial infection, an antibiotic, e.g. B. erythromycin ointment 1-2 times a day. Topical steroids can relieve acute symptoms but tend to prolong the course, particularly in the case of corneal infiltrates.4
Herpes Simple.This usually manifests as pain or foreign body sensation and reduced vision. Examination may show a tender preauricular nodule, a corneal dendrite that stains with fluorescein (acute HSV), or a cloudy, edematous patch on the cornea (disciform HSV). Treatment consists of topical trifluridine eight times a day for 5 to 7 days until the dendrite heals. Debridement of the dendrite with a cotton swab at the slit lamp may also speed healing.5The ability to distinguish between HSV keratitis and conjunctivitis is important. Immediate referral to an ophthalmologist is recommended.
Bacterial conjunctivitis.This presents with a history of yellowish discharge and twitching eyelids on awakening. It can be easy to difficult. Hyperacute or extremely severe cases of purulent conjunctivitis are often due to gonococci, which are also the only bacterial conjunctivitis with preauricular adenopathy. Examination reveals mild to severe conjunctival injection and purulent discharge. Most cases of bacterial conjunctivitis are mild and self-limiting. Treatment should be with an older generation antibiotic, such as 10% sodium sulfacetamide, 4 times daily for 5 to 7 days.6Due to emerging resistance issues, overuse of newer generation broad-spectrum antibiotics (such as topical fluoroquinolones) should be avoided.7Nonresponding infections should be cultured and treatment adjusted based on culture results. Gonococcal infection requires systemic treatment (ceftriaxone),8Eye rinse and topical erythromycin, along with appropriate reporting and treatment of partner.
Bacterial keratitis.Patients have a history of photophobia, pain, and decreased vision. It is more common in soft contact lens wearers, especially if the lenses are worn overnight. The patient may have had a predisposing lesion to the corneal epithelium, such as B. an abrasion from minor trauma or misaligned eyelashes. Physical examination shows marked conjunctival injection, whitish superficial corneal ulcer, anterior chamber reaction, and occasionally a hypopyon. Obtain an ophthalmologist consultation for a culture and scraping of the cornea and possible hospital admission. Treatment usually begins with broad-spectrum topical antibiotics 24 hours a day, every hour. One of the fluoroquinolones (oflaxacin or ciprofloxacin) is usually used initially, and the drugs are adjusted based on culture results.9Homatropin 5% bid helps reduce ciliary spasms and pain.
fungal keratitis.The symptoms are similar to bacterial keratitis. Examination shows a more delicate aspect of the corneal infiltrate and should be referred to an ophthalmologist. There is often a history of superficial corneal injury from plant matter. Treat patients with natamycin drops after obtaining cultures. Fungal ulcers may require surgical debridement.
Endoftalmitis.History of recent intraocular surgery or trauma (usually within 48 to 72 hours). There is usually a sudden decrease in vision with hand movements or light perception. Examination reveals marked conjunctival injection, discharge, possible eyelid edema, cloudy cornea, and marked anterior chamber cellular response with hypopyon. In the case of inflammation of the vitreous, the back of the eye is often not visible. Endophthalmitis is a true eye emergency and requires immediate evaluation and treatment by an ophthalmologist. Treatment consists of vitreous biopsy or vitrectomy, intravitreal antibiotics and possibly steroids, and intensive topical antibiotics. The prognosis depends on the causative organism and the duration of treatment.10
Infections of the eyelids (preseptal cellulitis).There is a history of spontaneous onset or recent mild eyelid trauma. Examination reveals a red, edematous eyelid. The balloon is normal to slightly injected. Vision, extraocular motility, pupils, and optic disc are usually normal. Look for a sty (infection at the base of the eyelashes) or a chalazion (enlarged meibomian gland) as a triggering event. Use qid warm compresses if there are signs of a chalazion. If there is early infection and Gram stain material is not available, treat empirically with amoxicillin/clavulanic acid 250-500 mg orally. 3 times a day in adults and an appropriately adjusted dose in children.11More severe cases may require incision and drainage of the eyelid and treatment with appropriate IV antibiotics based on Gram stain and culture. A careful distinction must be made between preseptal and orbital phlegmon.
Orbital cellulitis.Patients report pain, decreased vision, and possible diplopia. You may have sinusitis (especially ethmoiditis), recent orbital trauma, or recent dental surgery. Examination reveals swollen and erythematous eyelids, mild to severe proptosis, restricted MOEs, decreased vision, and possible afferent pupillary defects. Evaluation includes a CT scan (look for signs of sinusitis, subperiosteal abscess, and orbital abscess) and appropriate cultures. Patients are admitted and receive broad-spectrum care with intravenous antibiotics (clindamycin and ceftazidime). An otolaryngology consultation should be obtained.12In diabetics with ketoacidosis and immunocompromised patients, a life-threatening fungal infection (mucormycosis) should be considered, requiring immediate treatment with IV, amphotericin B, surgical debridement, and possibly hyperbaric oxygen.13
Dacryozyktitis.Patients report purulent discharge and pain in the medial region of the eyelid. Examination shows swelling and erythema in the lacrimal sac area and often reflux discharge through the puncta with pressure on the lacrimal sac. Treat by collecting cultures and starting oral antibiotics (amoxicillin/clavulanic 250 to 500 mg po 3 times daily or cephalexin 500 mg po every 6 hours). The definitive treatment is surgical dacryocystorhinostomy.14
Uveitis or inflammation of the uveal tissue (iris and choroid).The most common manifestation is iritis. There is a history of pain, photophobia, and decreased vision. Examination shows ocular injection, particularly at the corneal-scleral limbus, and whitish deposits on the posterior cornea (keratic precipitates). Flashes and cells can be seen in the anterior chamber with a tangential slit beam. There may be a hypopyon and dilated vessels in the iris. Fundus examination is required to rule out posterior uveitis. Intraocular pressure can be increased by inflammatory cells or decreased by inflammation of the ciliary body. In the case of isolated primary acute iritis, laboratory tests are often not necessary. Treatment with intensive topical steroids (1% prednisolone acetate every hour) and cycloplegics (1% atropine or 5% homatropine twice daily).quinceOphthalmologic follow-up is required for steroid taper and further diagnostic studies, particularly if there is evidence of posterior (choroidal) involvement.
Acute angle glaucoma.Patients usually present with sudden flushing, decreased vision, severe pain, and possible nausea and vomiting. This is more common in farsighted patients. Examination shows significant ocular injection, particularly at the limbus. The cornea is edematous. The pupil may be moderately dilated and unreactive. Intraocular pressure rises, often significantly to 60 or 70 mmHg. The other eye is also at significant risk of angle closure and can be examined for narrow angles with the slit lamp. Angle closure is a true ophthalmological emergency that requires immediate attention. Eye massage should be done immediately, as this can sometimes interrupt the attack. Local aqueous suppressants (timolol, brominidine, dorzolamide) are placed in the eye. Miotics such as 2% pilocarpine are given. Oral osmotics, such as 50% glycerol, are given to lower intraocular pressure. Surgical (laser or incision) peripheral iridectomy is performed as soon as possible. Prophylactic peripheral iridectomy is usually placed in the other eye within 1 to 2 weeks.sixteen
Cavernous carotid fistula.There are two main types, low flow and high flow. The low flow type is usually found in elderly hypertensive patients with no history of trauma. They present with a red eye due to dilation of the episcleral vessels, increased intraocular pressure, and possibly proptosis. Treatment is monitoring and observation of blood pressure or, in the most severe cases, interventional radiology. High-flow types are usually found in younger patients after blunt or penetrating head injuries. Vision may be reduced. Externally and internally there is marked ocular vascular swelling and usually marked exophthalmos. This requires emergency treatment. Interventional radiological treatment methods are often used with an attempt at embolic closure of the fistula.17
traumatic vision loss
Acid burns.Chemical exposure of the eye is a true eye emergency. A quick and vigorous rinse is essential for a successful treatment. IV solutions such as B. Ringer's or normal saline connected to a large diameter IV line may be used to irrigate the eye at a rate of 500 cc/30 minutes. The eye should be kept open and topical anesthesia with proparacaine or tetracaine is recommended to facilitate lavage. Special irrigation contact lenses are sometimes used, but this is not necessary. Care should be taken to ensure that the patient moves the eye in all directions and careful inspection of the fornix should be made during lavage. Five minutes after the end of the wash, the pH of the eye should be checked and the pH range should be between 6.8 and 7.4. If the pH falls outside of this range, additional watering is required.
It is essential to have a complete history of the incident, identifying the chemical and duration of exposure prior to irrigation. (See Table 3.) Acids cause surface proteins to precipitate and coagulate, confining the chemical to the surface of the eye and limiting damage. The most common causes of acid damage are sulfuric, sulfuric, hydrofluoric, acetic, chromic, and hydrochloric acids.18Alkalis saponify and dissolve cell membranes, allowing penetration into the eye and causing significant damage deep within the eye. The most common causes of alkali damage are ammonia, bleach, potassium hydroxide, magnesium hydroxide, and lime.18In all chemical injuries, a comprehensive eyelid examination with eversion of the eyelids to examine the fornixes for abnormalities is important. Calcium hydroxide particles are easier to remove with an EDTA-soaked cotton swab. A slit-lamp examination of the cornea and conjunctiva with fluorescein is necessary to check for discoloration defects in the cornea. Intraocular pressure should be checked with the tonopen or Goldmann applanation tonometer. At this point, immediate referral to an ophthalmologist is recommended. If the pressure in the eye is high, Diamox 250 mg tablets and a drop of a topical beta-blocker such as Timoptic 0.5% will help to reduce the pressure. Cycloplegic drop (0.25% scopolamine) and topical antibiotic ointment (erythromycin) should be administered along with oral pain control medications.
|Table 3. Common Chemical Substances Involved in Eye Injuries|
|battery acid||sulfuric acid (H2SO4)||acid|
|whitening||Sulfurous acid (H2WHAT'S MORE3)||acid|
|cement and mortar||Calcium (Ca(OH)2||Alkali|
|chrome solution||Chromic acid (Cr2o3)||acid|
|drain cleaner||Lauge (NaOH)||Alkali|
|glacial acetic acid||acetic acid (CH3COH)||acid|
|Glass and tile cleaner||Ammonia (NH3)||Alkali|
|acid for glazing||hydrofluoric acid||acid|
|hydrochloric acid||hydrochloric acid||acid|
|industrial cleaner||sulfuric acid||acid|
|flares and firecrackers||magnesium hydroxide||Alkali|
|Vinegar||acetic acid (ch3COH)||acid|
Trauma to the eyelids and orbit can pose a serious threat to vision. The history should contain relevant information on blunt and sharp objects, object type, and object speed. A complete examination of the eyelids, globe, motility, and palpation of the orbital rim is important. The presence of eyelid tears requires careful cleaning of the wound and determination of tissue loss. Unless the patient comes with tissue in a plastic bag, tissue loss is rare, even in a complex eyelid injury involving multiple full-thickness skin lesions with significant globe exposure. Great care must be taken not to discard tissue or remove apparently macerated tissue from the lid surface. If the lesion is lateral to the puncta, the probability of a canalicular lesion is low. If the lesion is medial to the puncta and involves the eyelid margins, the possibility of a canalicular lesion exists. For all lesions at the lid margins and/or medial lid, an experienced ophthalmologist or facial plastic specialist should close the wound, taking care to maintain the integrity of the canal system with stenting. Repair of eyelid injuries should be considered urgent, and in most cases a delay of 12 to 36 hours does not change the outcome of the operation.19Lid tears lateral to the puncta can be easily closed with 6.0 nylon or silk suture superficially and 6.0 Vicryl for deeper structures, such as the tarsal plate. Care should be taken to close lesions horizontally as often as possible, as vertical closure can lead to scarring ectropion with exposure and dry eyes. Prophylactic antibiotics are indicated when administered within three hours of injury, but because the eyelids are highly vascularized, the likelihood of infection is reduced and most eyelids thrive.20
If examination of the orbital walls with careful palpation reveals crepitus, subcutaneous air, or severely impaired ocular motility, further evaluation with orbital CT scanning is indicated to rule out orbital fractures.21Orbital fractures are commonly seen with blunt trauma to the orbit. A careful examination of the eye by an ophthalmologist prior to surgery is important, and the presence of diplopia with restricted mobility should be determined. The distinction between a paretic muscle and a pinched muscle that limits mobility (leash effect) is important. The timing of repair is controversial, with some experts suggesting an initial aggressive surgical repair.22,23and others suggest delaying the repair until the orbit is reassessed in 10 to 14 days.24Inferior orbital fractures require repair only if there is diplopia within the central 20° of vision, significant enophthalmos, or recession of the globe into the maxillary sinus. Too often, surgery is done immediately so that the orbital edema does not have time to subside so that a better assessment of motility can be made.
intraorbital foreign body
If an orbital foreign body is detected on a CT scan or X-ray, an accurate medical history is extremely important to determine the type of foreign body. If the foreign body is made of organic material, such as wood or plant matter, it must be removed to prevent orbital cellulitis. Copper residues are not well tolerated and must also be removed. Brass and bronze copper alloys are fairly well tolerated and inert substances such as glass, plastic, iron, lead, steel and aluminum are well tolerated and can be left in orbit. BBs and pellets are usually made up of 80-90% lead and 10-20% iron.
corneal foreign bodies
Corneal foreign bodies are the most common workplace injuries, accounting for nearly 35% of all workplace eye injuries.25There is usually a history of grinding wheel work or metal-to-metal contact. A complete examination of the cornea and anterior chamber with a slit lamp is mandatory to rule out intraocular foreign bodies. Careful examination of the conjunctiva under the upper and lower lids down to the fornix is necessary to remove particles trapped in the eyelid conjunctiva. Superficial foreign bodies can be removed by washing, but foreign bodies embedded in the cornea should be removed by slit lamp with a 25-gauge needle or foreign body extractor. Residual rust and material must be removed with a foreign body cutter. If the foreign body is in the visual axis, it would be advisable to see an ophthalmologist to remove the foreign body in order to limit the size of the scar and thus reduce the risk of vision loss. After removal, a cycloplegic (1% Cyclogyl) and broad-spectrum antibiotic ointment are administered to prevent infection of the cornea until the defect has healed.
Intraocular foreign bodies
Patients with a history of trauma from a sharp object or high velocity projectile are at high risk of corneal injury and possible intraocular foreign body. Signs such as a shallow anterior chamber, subconjunctival hemorrhage, hypotension, hyphema, cataracts, and decreased vision may indicate a ruptured globe. Thin-cut orbital CT scans are the gold standard for detecting intraocular foreign bodies. The presence of an intraocular foreign body on CT scan requires urgent referral to an ophthalmologist. The eyeball should not be manipulated excessively and eye protection should be put on. Substances such as copper, iron, steel, and organic matter must be removed immediately due to the risk of retinal toxicity or endophthalmitis. (See Table 4.) Patients should undergo pars plana vitrectomy and foreign body removal.26The prognosis for vision is poor, especially if the foreign body has become embedded in the retina due to the risk of proliferative vitreoretinopathy (PVR).27In patients with PVR, significant scar tissue develops on the retinal surface and can lead to traction-induced retinal detachment with poor visual outcomes. All patients with an intraocular foreign body have a lesion in the cornea or sclera and require surgical repair of the lesion. (Consult Lesions of the cornea and sclerotia, page 253.)
|Table4. Commonly encountered intraocular foreign bodies|
|foreign body class||exercise||administration|
|copper||highly flammable||remove immediately|
|Eisen||severe inflammatory reaction||remove immediately|
|Organic – wood, plants and cilia||highly flammable||remove immediately|
|Stahl||highly flammable||remove immediately|
Corneal abrasions and erosions
In patients who complain of severe pain, erythema with edema of the eyelids, and photophobia, a corneal abrasion should be considered in the differential diagnosis. The patient may report a history of trauma, contact lens wear, herpes infection, or sharp pain on awakening. Patients should be examined with the slit lamp using single light and cobalt blue light with fluorescein dye in a topical anesthetic. If there is an epithelial defect, it absorbs the dye and fluoresces yellow against blue background light. The examiner should make the patient blink. If the dye accumulates without abrasion, the yellow fluorescein will dislodge. When scratched off, the yellow fluorescein area remains attached to the cornea. Care must be taken to distinguish between a corneal abrasion and the visible dendrite within it.Herpes-Keratitis. Treatment with broad-spectrum antibiotic drops (10% Sulfacetamide or Polytrim) and cycloplegic drops (1% Cyclogyl) is recommended. Currently there are important questions about the advantages of a pressure patch over no patch.28,29If patients do not receive a patch, topical non-steroidal agents such as diclofenac or ketorolac are recommended for pain control.30,31Contact lens abrasions require gram-negative coverage with an aminoglycoside and a cycloplegic without a patch. These abrasions must be carefully monitored to ensure that a corneal ulcer does not develop.
Patients with acute onset of pain and redness on awakening often have a history of a previous major corneal abrasion. In these patients, the adhesion complexes between the epithelium and the basement membrane were damaged, leading to recurrent corneal erosions. Slit-lamp examination reveals a full-thickness epithelial defect or epithelial irregularity with motile epithelium. The epithelium must be debrided and the treatment is the same as for a corneal abrasion. After the epithelium has healed, abundant lubrication is required for 6-8 weeks, especially at night, a lubricating ointment. If the erosions reappear, surgical intervention is required to increase the adhesion complexes.
Sometimes conjunctival injury occurs only with careful examination of the globe in patients with mild pain, red eyes, foreign body sensation, and a history of trauma. Exploration of the site and possible CT scan of the orbit may be indicated to rule out ocular rupture. Lesion confined to the conjunctiva heals rapidly and may require antibiotic ointment for 4 to 7 days. Large lacerations (>1.5 cm) can be sutured, but most do not require surgical repair. These patients should be re-evaluated within a week if the injury is significant.
Corneal and scleral injuries
Injuries to the eyeball can be caused by blunt trauma, projectiles, or sharp objects. The sclera and cornea are normally resistant to blunt trauma, but rupture of the sclera can occur with sufficient force. Compressive forces rarely cause rupture at the point of impact, but ruptures occur at a distant location where the sclera is thinnest. The sclera is thinnest at the junction of the cornea and sclera (limb) and behind the insertion of the rectus muscles. Scleral ruptures generally occur in the superonasal and superotemporal quadrants, are solitary, and extend from the limbus to the equator of the globe. Bullet and sharp object injuries occur primarily in the front of the eye and can affect both the cornea and sclera. Signs of rupture include hyphema, cataract, vitreous hemorrhage, visual acuity with or without light perception, ocular hypotension, and subconjunctival hemorrhage. If injury to the cornea and sclera is suspected, place a shield over the eye and, if one is not available, do so with the bottom of a Styrofoam cup and consult an ophthalmologist immediately. Do not attempt to stop the exam as this may result in further extrusion of the contents of the eye. An orbital CT scan is highly recommended to rule out intraocular foreign bodies, and prompt surgical repair with appropriate ophthalmic follow-up is required. Lesions larger than 20 mm and those caused by blunt trauma or projectiles usually have a poor visual prognosis.32After primary tear repair, vitreoretinal surgery to reattach the retina or remove retinal traction has significantly improved visual outcomes.33
Traumatic iritis and hyphema
The four phases of a blunt injury are compression, decompression, overdrive, and oscillations.34Anteroposterior compression causes equatorial expansion, shortening of the visual axis, and posterior displacement of the lens and iris. Extreme stretching of ocular tissue causes specific types of injury to the iris, trabecular meshwork, ciliary body, lens, vitreous, retina, choroid, sclera, and optic nerve. The net result can be a breakdown of the blood-water barrier and the blood-retina barrier. Depending on the extent of the damage, traumatic uveitis or traumatic hyphema may occur.
If the patient complains of pain, photophobia, and tearing, a careful slit-lamp examination should be performed to look for an anterior flash (protein) and cells (white blood cells). Because the signs of uveitis can be subtle, referral to an experienced ophthalmologist is preferred.
Flash and cell in the anterior chamber indicate traumatic uveitis, which has a short and benign course.35Cycloplegic eye drops (Cyclogyl 1% 4 times a day) and prednisone eye drops (Prednisolone acetate 1% 4 times a day) for one week reduce inflammation and a re-evaluation of the eye is recommended in one week.
Patients with blood in the anterior chamber or on slit-lamp examination have hyphema. These patients deserve a thorough examination by an ophthalmologist to rule out the possibility of a ruptured globe. There is a high risk of rebleeding within five days of the initial trauma and increased intraocular pressure. In the past, patients have been hospitalized for hyphema, but there does not appear to be a significant difference in the rate of rebleeding and clinical outcomes between hospitalized and home-treated patients.36,37Close-knit outpatient follow-up care and strict bed rest are necessary to prevent postoperative bleeding.38Cycloplegia with atropine 1% twice daily and topical steroids (prednisolone acetate 1% four times daily) are administered to improve patient comfort but have not been shown to prevent rebleeding or improve outcome. Antifibrinolytics, such as aminocaproic acid, can be used both systemically and topically to stabilize the clot for 5 days and reduce the rate of rebleeding.39-41Patients with hyphema should be evaluated daily for rebleeding and increased intraocular pressure 5 days after trauma and then 2 days after stopping aminocaproic acid. About 5% of patients with hyphema develop uncontrollable intraocular pressure, prolonged clotting time, and blood spotting on the cornea. These patients require surgery to remove the clot from the anterior chamber. Great care is needed to avoid vision loss from uncontrolled glaucoma or blood spots on the cornea, and pressure control is essential.
Retinal edema, retinal tear, and vitreous hemorrhage
Traumatic forces can cause violent movement of the vitreous away from the retina, resulting in a blow or counter-blow injury to the retina. The most common types of injuries are retinal tears and non-tear retinal injuries that cause retinal edema or retinal hemorrhage.42Retinal edema, called Berlin edema or commotio retinae, can be seen at the periphery of the retina or at the posterior pole. When it comes to the macula or fovea, the patient often complains of decreased vision due to photoreceptor dysfunction.43Direct ophthalmoscopy may show a gray-white central retinal lesion that is difficult to detect without extensive examination. Patients who have suffered a blunt retinal trauma do not require emergency surgery, but follow-up by the ophthalmologist is required because they may develop sequelae such as atrophy of the retinal pigment epithelium or macular hole.44If a macular hole develops, surgery to repair the hole should be considered. Retinal hemorrhages should be observed and will reabsorb over time. They usually do not cause chronic vision loss.
Occasionally, patients complain of decreased vision and poor vision of the retina. If the vitreous detaches from the retina and a retinal vessel ruptures, vitreous hemorrhage may occur, making ophthalmoscopic evaluation of the retina impossible. If there is no rupture of the eyeball, vitreous hemorrhage should be carefully monitored with diagnostic ultrasound, called a B-scan, to rule out retinal tears or detachments. Patients should be monitored monthly until bleeding resolves. Some retina specialists would perform a vitrectomy before six months to improve vision and prevent other complications if vitreous hemorrhage continues.
Traumatic retinal tears occur most often at the leading edge of the retina, at its junction with the ciliary body, and are known as retinal dialysis.45Often, due to its location, the retinal dialysis is not visible at the time of injury and may go undetected on subsequent investigations. Many retinal detachments associated with retinal dialysis are not diagnosed until more than a year after the injury. The inferotemporal and superonasal quadrants are most commonly affected.46A careful history and follow-up examination can prevent the progression of a retinal detachment. If a retinal tear is noted, laser photocoagulation or freezing therapy will stabilize the retina. Patients with prior trauma, flashing lights, and a gray curtain over the eye are at high risk for retinal detachment. Immediate referral to an ophthalmologist for indirect ophthalmoscopic examination could prevent further delays in diagnosis and surgical repair. The visual prognosis is good if the retinal breaks or detachments are diagnosed and repaired within six weeks after surgery.47The patient may undergo an air insertion, scleral buckling, or pars plana vitrectomy to repair a retinal detachment.
The compressive forces of trauma can cause dehiscence of the zonules that support the lens. A decentration of the lens with partial zonular dehiscence is called a subluxation. Total zonular dysfunction can lead to dislocation of the lens into the vitreous cavity or into the anterior chamber. The lens capsule is usually intact and inflammation is minimal. In most cases, observation and a complete eye examination with refraction are sufficient for visual rehabilitation. However, in the case of subluxed lenses with a lens edge in the visual axis or dislocated lenses with angle-closure glaucoma, surgical intervention is necessary. Although intracapsular lens extraction is still used by many ophthalmologists, pars plana lens extraction has yielded promising results.48
optic nerve trauma
Patients with optic nerve injury may have reduced visual acuity, visual field defects, or a relative afferent pupillary defect. Examination of the pupils with the swinging flashlight test should be performed, but it is sometimes difficult to evaluate the injured eye due to corneal opacity, hyphema, or eyelid edema. In this case, checking the consensus response in the other eye helps the examiner determine the condition of the nerve. Nerve trauma can be direct, e.g. B. penetrating injuries from projectiles or objects that tear the nerve. Orbital fractures and high velocity bullets can also cause severe nerve pinching. The first due to compression by bone fragments and the second due to significant energy dissipation in the vicinity of the nerve. Increased tissue pressure from orbital air or retrobulbar hemorrhage can cause optic nerve compression, and traction forces on the eyeball can tear the optic nerve completely out of the eye.49,50Disc edema, hemorrhage, or avulsion can usually be seen on ophthalmoscopy.
Indirect trauma can occur when there is no initial ophthalmoscopic evidence of injury to the eye. Often the severity of the injury is not proportional to the degree of vision loss and may be immediate or delayed. The concussion forces cutting axons at the cribriform plate where the nerve enters the eye. Optic atrophy with pale optic nerve is seen after 3 to 6 weeks. In general, the prognosis for recovery of vision from traumatic optic nerve injury is poor, but intravenous corticosteroids given for 3–5 days have been shown to be beneficial. Treatment must be started immediately.
Non-traumatic vision loss
Non-traumatic acute vision loss poses particular diagnostic challenges. Important historical points include time of onset, quality and severity of vision loss, mono or binocularity, duration of loss, and associated ocular and systemic diseases. It is helpful to think of the structure of the globe from anterior to posterior in order to classify the various etiologies of nontraumatic acute vision loss. Corneal causes include corneal erosions (which may occur spontaneously or be associated with corneal epithelial dystrophy or bullous keratopathy), infectious keratitis, or toxic reactions to chemicals or drugs. Anterior chamber causes include acute iritis and spontaneous hyphema. Lenticular causes include cataracts (usually a posterior subcapsular type that progresses quite rapidly and may be noticed "suddenly" by the patient). Vitreous causes include spontaneous vitreous hemorrhage (common in diabetics with proliferative retinopathy) or pars planitis (idiopathic vitreous inflammation that usually occurs in young adults).
Retinal and optic nerve disorders are probably the most common causes of non-traumatic acute vision loss. (See Table 5.) Central retinal artery occlusion requires immediate ophthalmologic attention to try to preserve vision.
|Table5. Retinal causes of acute non-traumatic vision loss|
|history||Metamorphopsia to sudden loss of central vision, especially in the elderly||Episodes of fleeting amaurosis, sudden loss of vision, middle or old age||Rapid (over several days) to sudden loss of vision, usually in older people, but can also be seen in young adults.||dark shadow on vision, often preceded by flashes and floaters|
|visual acuity||small decrease in central vision loss||usually severe loss of finger counting or absence of light perception||moderate to heavy loss||normal to severe loss depending on macular status|
|students||no afferent defect||large afferent defect on affected side||often have an afferent defect||afferent defect depending on the size of the detachment|
|Retina||Drusen (yellow spots), pigment clumps, bleeding||milky swollen retina with a cherry red spot on the fovea, possibly Hollenhorst plaque||generalized retinal hemorrhages and white retinal infarcts||raised, whitish, wavy retinal tissue; tears can be seen in the retina|
|optic nerve||not affected||usually pale, may be swollen||swollen and blocked vessels with bleeding||normally normal - may darken from shedding|
|Referral for fluorescein angiography within 24-48 hours||immediate eye massage, previous IOP||Treat any paracentesis with IOP elevation chamber||Referral to ophthalmologist for repair.|
|Laser treatment of adequate lesions, poor long-term prognosis18||if not reversed acutely, the prognosis is very poor; beware of neovascularization19||close monitoring for neovascular complications, possible lasertx20||pneumatic retinopexy or scleral cerclage or vitrectomy used for repair21|
optic nerve disorders
Optic nerve dysfunction causes decreased visual acuity, decreased color vision, and almost always presents with an afferent pupillary defect. The optic nerve may appear swollen, congested, and possibly pale, or it may appear normal if the damage is retrobulbar. Optic neuritis is seen in younger patients (age group 15-45). Examination shows the above findings, and there may be pain with extraocular movements. Vision may drop to a low level and then usually recover, although often not completely. Treatment is based on the results of the Optic Neuritis Treatment Study. Oral steroids should not be used. In severe cases, high doses of intravenous steroids can help speed recovery.55Anterior ischemic optic neuropathy (AION) is more common in elderly patients. It is found in both arteritic (age > 55 years) and non-arteritic (age 45-65) forms. The arteritic form is associated with giant cell arteritis. Patients may have severe vision loss in one eye and associated central retinal artery occlusion. If left untreated, the second eye also has a significant chance of losing vision. Patients often present with temporal artery tenderness and systemic symptoms such as jaw claudication, weight loss, and fever. Westergren's sedimentation rate (> 47) and c-reactive protein level (> 2.45 mg/dL) can help in the diagnosis.56If a patient presents with a clinical presentation consistent with giant cell arteritis, high-dose systemic steroids should be started immediately and a temporal artery biopsy ordered. The non-arteritic form of anterior ischemic optic neuropathy is commonly found in patients with underlying systemic hypertension or diabetes mellitus. There is no proven treatment for non-arteritic AION.
Anisocoria, or a difference in pupil size, may be a benign physiologic condition or a sign of severe and life-threatening intracranial disease. Important historical items include any recent trauma, any previously noted anisocoria, foreign bodies in the eyes, and any headache, diplopia, or other neurologic symptoms. An efficient and accurate decision tree is shown in Figure 1. See an ophthalmologist if you have questions about the cause of the anisocoria. Any anisocoria associated with a third nerve palsy ("dilated pupil" on the ipsilateral side) requires emergency neuroradiologic evaluation and possibly emergency neurosurgical intervention if an intracranial aneurysm is found.57
Diplopia, or double vision, can be divided into binocular diplopia (present only when the eyes are open) or monocular diplopia (still present when the eyes are closed). Other important historical points are the time of onset, whether the diplopia is intermittent or constant, the gaze directions in which the diplopia worsens, previous trauma, and any previous eye surgery, particularly strabismus surgery. During the examination, pay special attention to the examination of the pupils and extraocular motility. Close your right eye first, then your left eye to see if there is any change or corrective movement. Rapidly changing the occluder between the eyes can also help induce abnormalities. Categorize eye alignment as normal, esotropic, exotropic, or vertical misalignment. Carefully examine the full range of extraocular movement to determine if there is visible muscle paralysis. If the patient finds that the diplopia is worse or is only present in certain directions of gaze, this can be a good indication of which muscles are not working properly. True monocular diplopia is usually caused by an abnormality in the cornea, lens, or central retina. A full dilated exam is usually required to find the cause. Children and young adults may have sixth nerve palsy after head trauma or a viral illness, or it may be an intracranial process. An intensive neuroimaging study is indicated.58Acute third nerve palsies with pupillary involvement in young or elderly adults may represent the effects of a posterior communicating artery aneurysm. Neuroradiological studies and multiple sclerosis can present in young adults with any pattern of EOM involvement, which can have a high degree of variability. Elderly patients often have sixth or fourth nerve palsy as a result of a microvascular accident. These patients often have hypertension, diabetes, or generalized atherosclerotic vascular disease. If they do not have other neurological findings and a history of predisposing disease, they can be observed for 3 to 4 months.59If they have other neurological findings, worsen, or show no improvement after 3 to 4 months, do an MRI. Acute onset of diplopia or worsening of diplopia in patients with Graves' disease may indicate new disease activity. This may require immediate evaluation and treatment (eg, radiation, orbital decompression, systemic steroids) if visual disturbances, increased intraocular pressure, or signs of optic nerve compression occur.
Patients presenting with ocular emergencies can present with a variety of conditions ranging from benign to vision-impairing and life-threatening. Accurate and timely diagnosis is required, and this requires careful slit lamp and ophthalmoscopic examination by the physician to determine if an emergency ophthalmologic consultation is needed. In patients with red eyes, the physician must be able to rule out site-threatening conditions before treating a patient for conjunctivitis. In case of traumatic loss of vision, the patient should be referred to an ophthalmologist immediately after an initial evaluation. In patients with suspected rupture of the eyeball or intraocular foreign body, an orbital computed tomography should be performed, eye protection placed, and the ophthalmologist to determine the extent of the lesion. Vision-damaging mistakes are typically only made when doctors attempt to treat eye emergencies without the help of an experienced eye care professional.
1. I met MD. Evaluation and initial management of patients with ocular and adnexal trauma. In: Albert DM, Jakobiec FA, eds.Principles and practice of ophthalmology. WB Saunders; 1994: 3367.
[ PubMed ] 2. Congdon NG, MacCumber MW. Ocular assessment In: MacCumber MW, hrsg.Management of eye injuries and emergencies.. Philadelphia, Pennsylvania: Lippincott-Raven; 1998:36.
3. Cullom RD, Chang B, eds.El manual de Wills Eye. 2. Aufl. Philadelphia, Pennsylvania: Lippincott-Raven; 1994: 119-120.
4. Berlin MW, et al., Hrsg.External Diseases and Cornea, Section 8, The Fundamental and Clinical Sciences Course. . . . . . . . . . . . . . . . San Francisco, CA: American Academy of Ophthalmology; 1993:97.
5. Harris LL, O'Brien TP. Infectious conjunctivitis and keratitis. In: MacCumber MW, ed.Management of eye injuries and emergencies.. Philadelphia, Pennsylvania: Lippincott-Raven; 1998:200.
6. Manis MJ. Bacterial conjunctivitis. In: Tasman W., Jaeger EA, eds.Duane Clinic Ophthalmology. Filadelfia, Pensilvania: JB Lippincott; 1994:4.
7. Knauf HP, et al. Sensitivity of corneal and conjunctival pathogens to ciprofloxacin.cornea1996; 1:66-71.
8. Authors are not listed. The choice of antibacterial drugsWith Light Drogas Ther1998;40(1023):38..
9. Hunduik RA, et al. Comparison of 3% ciprofloxacin ophthalmic solution with tobramycin-spiked cefazolin in the treatment of bacterial corneal ulcers. Ciprofloxacin-induced bacterial keratitis study group.ophthalmology1996;11:1854-1862
10. Endophthalmitis Vitrectomy Study Group. Results of the vitrectomy endophthalmitis study: a randomized trial of immediate vitrectomy and intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis.ophthalmol arc1995; 113: 1479-1496.
[ PubMed ] 11. Sadda SR, Iliff NT. Infections of the lacrimal system and orbit. In: MacCumber MW, ed.Management of eye injuries and emergencies., Philadelphia, Pennsylvania: Lippincott-Raven; 1998: 130.
[ PubMed ] 12. Sadda SR, Iliff NT. Infections of the lacrimal system and orbit. In: MacCumber MW, ed.Management of eye injuries and emergencies., Philadelphia, Pennsylvania: Lippincott-Raven; 1998: 132.
13. Nerad JA, et al., Hrsg.Orbit, eyelids and lacrimal system, Section 7, Basic and clinical sciences course. . . . . . . . . . . . . . . . San Francisco, CA: American Academy of Ophthalmology; 1995:6
14. Cullom RD, Chang B, eds.El manual de Wills Eye. 2. Aufl. Philadelphia, Pennsylvania: Lippincott-Raven; 1994: 143.
15. Rao NA y col., eds.Intraocular Inflammation and Uveitis, Section 9, Fundamental and Clinical Sciences Course. . . . . . . . . . . . . . . . San Francisco, CA: American Academy of Ophthalmology; 1995: 81-8
16. Simmons RJ, et al. Primary angle closure glaucoma. In: Tasman W., Jaeger EA, eds.Duane Clinical Ophthalmology, Band 3, Chapter 53. Filadelfia, Pensilvania: JB Lippincott; 1994: 13-14.
17. Troost BT, Glaser JS. Aneurysms, arteriovenous junctions, and related vascular malformations. In: Tasman W., Jaeger EA, eds.Duane's Clinical Ophthalmology Band 2 Chapter 17. Filadelfia, Pensilvania: JB Lippincott; 1994: 20-21.
18. Wagoner, MD. Chemical lesions of the eye: current concepts in pathophysiology and therapy.Surv Oftalmol1997; 41: 275-313.
[ PubMed ] 19. Rubin PA, Shore JW. Penetrating trauma of eyelid and orbit. In: Albert DM, Jakobiec FA, eds.Principles and practice of ophthalmology. WB Saunders; 1994: 3432.
20. West Fells CT, Shore JW. Isolated orbital floor fractures: risk of infection and role of antibiotic prophylaxis.eye surgery1991; 22:409-411.
21. Mucci B. A new perspective on blast fracture of the orbit.injury1997; 28: 555–556.
22. Levin LM, Kademani D. Clinical considerations in the management of orbital burst fractures.Compend Contin Educ Dent1997;18:596-598.
23. Bulls BS, et al. Oculocardiac reflex caused by a trapdoor fracture of the orbital floor: indication for urgent repair.ophthalmol arc1998; 116:955–956.
24. Seiff SR, Good WV. Hypertropia and posterior burst fracture: mechanism and management.ophthalmology1996; 103: 152-156.
25. Niceo T, et al. Analysis of 148 work accidents treated on an outpatient basis.Klin's Monthly Ophthalmology1996;209:7-11.
26. Kazokoglu H, Saatci O. Intraocular foreign bodies: results of 27 cases.ann oftalmol1990;22:373-376.
27. Cardillo JA, et al. Post-traumatic proliferative vitreoretinopathy. Epidemiological profile, appearance, risk factors and visual evolution.ophthalmology1997;104:1166-1173.
28. Hart A. et al. Management of corneal abrasions in accidents and emergencies.injury1997;28:527-529.
29. Patterson J., et al. Eye patch treatment for pain from corneal abrasion.Southern Mediterranean J1996;89:227-229.
30. Jayamanne DG, et al. The efficacy of topical diclofenac in relieving discomfort after traumatic corneal abrasions.Ojo1997; 11: 79-83.
31. Kaiser PK, Pineda R. A study of topical nonsteroidal anti-inflammatory drops and non-pressure patch in the treatment of corneal abrasions. Corneal Abrasion Patches Study Group.ophthalmology1997;104:1353-1359.
32. Esmaeli B. et al. Visual outcome and ocular survival after penetrating trauma. A clinicopathological study.ophthalmology1995; 102: 393-400.
33. Pieramici DJ, et al. Open balloon violation. Update on types of injuries and visual results.ophthalmology1996; 103: 1798-1803.
34. Hersh PS, et al. Anterior segment trauma. In: Albert DM, Jakobiec FA, Eds.Principles and practice of ophthalmology. WB Saunders; 1994: 3385–3390.
35. Seymour R, Ramsey MS. Unusually severe traumatic uveitis associated with occult ankylosing spondylitis.Can J Ophthalmol1991; 26:156-158.
36. Kennedy RH, Brubaker RF. Traumatic hyphema in a defined population.Soy J. Ophthalmol1988; 106: 123-130.
37. VG smart. Hyphema home care.ann oftalmol1982; 14:25-27.
38. Shiuey Y, Lucarelli MJ. Traumatic hyphema: results of outpatient treatment.ophthalmology1998;105:851-855.
39. Crouch ER, Frenkel M. Aminocaproic acid in the treatment of traumatic hyphema.Soy J. Ophthalmol1976;81:355-360.
40. Fourman S. Topical aminocarboxylic acid in the management of patients with traumatic hyphema.ophthalmol arc1998; 116: 395-396.
41. Crouch ER Jr., et al. Topical aminocaproic acid in the treatment of traumatic hyphema.ophthalmol arc1997; 115: 1106–1112.
42. Williams DF, et al. Posterior segment manifestations of ocular trauma.Retina1990; 10:35-44.
43. Liem AT, et al. Reversible lesion of the cone photoreceptor in macular retinal shock.Retina1995; 15:58-61.
44. Yanagiya N. et al. Clinical characteristics of traumatic macular holes.Jpn J Ophthalmol1996;40:544-547.
45. Ross W.H. Traumatic retinal dialysis.ophthalmol arc1981;99:1371-1374.
46. Zion VM, Burton TC. retinal dialysis.ophthalmol arc1980;98:1971-1974.
47.Johnston PB. Traumatic retinal detachment.Br J Oftalmol1991;75:18-21.
48. Omulecki W. et al. Pars plana vitrectomy, lensectomy, or removal for fixation of transscleral intraocular lenses to treat displaced lenses in a family with Marfan syndrome.Ophthalmic surgical lasers1998; 29:375–379.
49. Espaillat A, bis K. Various veins.ophthalmol arc1998; 116: 540-541.
50. Tsopelas NV, Arvanitis PG. Optic disc avulsion after orbital trauma.ophthalmol arc1998; 116:394.
51. Macular Photocoagulation Study Group. Argon laser photocoagulation in neovascular maculopathy. Results of five years of randomized clinical trials.ophthalmol arc1991; 109: 1109-1114.
52. Heckenlively JR, et al., Eds.Retina and Vitreous Body, Section 12, Basic and Clinical Sciences Course. . . . . . . . . . . . . . . . San Francisco, CA: American Academy of Ophthalmology; 1995: 185–188.
53. Central Vein Occlusion Study Group. A randomized clinical trial of early panretinal photocoagulation in ischemic central vein occlusion. The central vein occlusion study report N.ophthalmology1995; 102: 1434–1444.
54. Cullom RD, Chang B, eds.El manual de Wills Eye. 2. Aufl. Philadelphia, Pennsylvania: Lippincott-Raven; 1994:250.
55. Beck RW, et al. A randomized controlled trial of corticosteroids for the treatment of acute optic neuritis.N incl. J Med1992; 326:581-588.
56. Hayreh SS, et al. Giant cell arteritis: validity and reliability of different diagnostic criteria.Soy J. Ophthalmol1997; 123:285-296.
57. Kerrison JB, Miller NR. Traumatic and other acute disorders of eye movements and pupils. In: MacCumber MW, ed.Management of eye injuries and emergencies.. Philadelphia, Pennsylvania: Lippincott-Raven; 1998: 370-371.
[ PubMed ] 58. Bayandas FJ, Kline LB. Handbook of neuroophthalmology review. 3rd edition Thorofare, New Jersey: Slack; 1988:8
[ PubMed ] 59. Bajandas FJ, Kline LB. Handbook of neuroophthalmology review. 3rd edition Thorofare, New Jersey: Slack; 1988:8
Eye emergencies include cuts, scratches, objects in the eye, burns, chemical exposure, and blunt injuries to the eye or eyelid. Certain eye infections and other medical conditions, such as blood clots or glaucoma, may also need medical care right away.Which of the following eye disorders are considered ocular emergencies? ›
All ocular emergencies, including a penetrating globe injury, retinal detachment, central retinal artery occlusion, acute angle-closure glaucoma, and chemical burns, should be referred immediately to the emergency department or an ophthalmologist.What is ophthalmic diagnosis? ›
Ophthalmic diagnostics are fluorescent substances known as disclosing agents, which help diagnose and treat certain eye conditions. A fluorescent orange dye is applied on the surface of the eye to visualize damage to the cornea, or foreign bodies in the eye.Why do we cover both eyes in an emergency involving one eye? ›
Covering both eyes helps prevent eye movement. If the object is large, place a clean paper cup or something similar over the injured eye and tape it in place. This prevents the object from being pressed on, which can injure the eye further. Get medical help right away.What are the five 5 usual common emergencies? ›
- Bleeding. Cuts and wounds cause bleeding, but severe injury can also cause internal bleeding that you can't see. ...
- Breathing difficulties. ...
- Someone collapses. ...
- Fit and/or epileptic seizure. ...
- Severe pain. ...
- Heart attack. ...
- A stroke.
The leading causes of blindness and low vision in the United States are primarily age-related eye diseases such as age-related macular degeneration, cataract, diabetic retinopathy, and glaucoma.What are the 3 common eye defects? ›
Refractive errors, including nearsightedness, farsightedness and astigmatism, are the most common causes of vision loss.What are the five most common vision related problems? ›
- Blurred vision (called refractive errors)
- Age-related macular degeneration.
- Diabetic retinopathy.
Mild – visual acuity worse than 6/12 to 6/18. Moderate – visual acuity worse than 6/18 to 6/60. Severe – visual acuity worse than 6/60 to 3/60. Blindness – visual acuity worse than 3/60.What are some common problems diagnosed from eye checkups? ›
- High blood pressure. ...
- Heart disease. ...
- Diabetes. ...
- Rheumatoid arthritis. ...
- Thyroid disorder. ...
- Parkinson's disease. ...
- Cancer. ...
- Multiple sclerosis.
A standard ophthalmic exam is a comprehensive series of tests done by an ophthalmologist or optometrist. These doctors specialize in eye health. They'll use these tests to check both your vision and the health of your eyes. A standard ophthalmic exam is also known as a comprehensive eye exam or a routine eye exam.What are ophthalmic symptoms? ›
- Decrease in vision.
- Halos or glare from lights, especially while driving at night.
- Eye pain or redness.
- Double vision.
- Dryness or excessive tearing.
- Eyelid abnormalities.
This is considered a medical emergency because the intraocular pressure spikes suddenly to anywhere from 30-70 mm or higher. This causes extremely sharp pain, nausea and vomiting, and cloudy vision. The IOP needs to be lowered within hours to prevent permanent vision loss.What is the first aid for an eye trauma? ›
IMPACT INJURY TO THE EYE
DO NOT rub or apply pressure to the eye. GENTLY APPLY a small cold compress to reduce pain and swelling. Even a light impact can cause severe injury to the eye. If swelling, discoloration (black eye), pain or visual disturbance occurs, immediately seek medical attention.
Sudden Total or Near-Total Vision Loss
Your doctor may call it “central retinal artery occlusion” or “branch retinal artery occlusion.” It also means you're at risk for a stroke or heart attack. It can happen if you get a blood clot that clogs a blood vessel in the eye.
- No breathing or difficulty breathing.
- No pulse.
- Severe bleeding.
- Financial emergency.
- Earthquake. ...
- Storm hurricane/snow. ...
- Flood. ...
- Fire. ...
- Accident. ...
- Medical emergency. ...
- Car breakdown/stranded. Admittedly, this does seem like a minor emergency. ...
The two most common defects of vision are myopia and hypermetropia. Myopia can be corrected by using a concave lens and hypermetropia can be corrected by using a convex lens.What are the two major eye defects? ›
As we saw earlier, the two major defects of eyes are nearsightedness and farsightedness. Myopia is the name of the condition for when a person is suffering from nearsightedness. This type of eye defect arises in a person because the power of the eye becomes too large.What neurological disorders cause eye problems? ›
- Optic Neuropathies. Damage to the optic nerves can cause pain and vision problems, most commonly in just one eye. ...
- Optic Neuritis. ...
- Giant Cell (Temporal) Arteritis. ...
- Chiasm Disorders.
- Dry Eye. Dry eye is one of the most common eye problems. ...
- Diabetic Retinopathy. Retinopathy is the most common eye problem in people with diabetes. ...
- Cataracts. As we age, the lenses in our eyes can become cloudy. ...
- Glaucoma. ...
- Macular Degeneration.
The four most common refractive errors are: myopia (nearsightedness): difficulty in seeing distant objects clearly; hyperopia (farsightedness): difficulty in seeing close objects clearly; astigmatism: distorted vision resulting from an irregularly curved cornea, the clear covering of the eyeball.What are the most common eye infections? ›
Conjunctivitis is the most common eye infection to present to primary healthcare providers and rarely threatens vision. Corneal infection (keratitis) and endophthalmitis are less common but pose a serious risk to vision.What are the indicators of visual impairment? ›
not be able to see objects at a distance, like on a whiteboard or blackboard. having trouble reading (or learning to read) and participating in class. not be able to focus on objects or follow them, may squint often and rub their eyes a lot, have chronic eye redness or sensitivity to light.What does Category 5 blindness mean? ›
Very severe blindness – visual impairment category 5 in one eye and no visual impairment in the other eye. • Total blindness – visual impairment category 6 in one eye and no visual impairment in the other eye. H54.5. Moderate visual impairment in one eye of a person.What are the three types of visual acuity? ›
- SPATIAL ACUITY: ability to resolve 2 points in space. ...
- TEMPORAL ACUITY: ability to distinguish visual events in time. ...
- SPECTRAL ACUITY: ability to distinguish differences in the wavelength of the stimuli.
These refractive errors are the most common eye problems in the U.S. Refractive errors include nearsightedness (myopia), farsightedness (hyperopia) and distorted vision at all distances (astigmatism). These eye conditions can be helped with eyeglasses, contacts or surgery.Can an eye exam detect neurological problems? ›
When a brain tumor forms and causes swelling and increased pressure in the brain, your optometrist can see its impact in the back of your eye. There may also be pressure on the optic nerve that your eye doctor can detect.What is eye scotoma? ›
A scotoma is a blind spot in your vision: i.e., an area you cannot see. Blind spots may be small or large and can be temporary or permanent. A scotoma can also move around to different places in your visual fields. Vision depends on the cornea and lens in your eye letting in light to form an image on the retina.What is the most common surgical ophthalmologic procedure? ›
LASIK — Perhaps the most well-known of eye surgeries, LASIK (short for Laser-Assisted In Situ Keratomileusis) uses a laser to reshape the cornea to correct nearsightedness, farsightedness, and astigmatism.
The neuro exam allows you to assess structures neighboring those that are important to vision and can help determine the level of urgency for a patient's ocular findings such as visual field defects, cranial neuropathies, double vision, optic neuropathy, ptosis, pupillary abnormalities and loss of vision.Why is it important that they have a comprehensive ophthalmologic examination yearly? ›
Many eye conditions — potentially blinding ones — don't have early symptoms. And some serious diseases that affect other systems in the body can first be diagnosed by an ophthalmologist. That is why it's important to have a complete eye examination once a year.What are ophthalmic complications? ›
Abstract. Ophthalmic complications are rare following maxillary osteotomies. Potential complications include a decrease in visual acuity, extraocular muscle dysfunction, neuroparalytic keratitis, and nasolacrimal problems involving both an increase or a decrease in tearing.What are the first signs that glaucoma is developing? ›
- Hazy or blurred vision: Distorted or blurry vision accompanied by other symptoms.
- Eye pain: Severe pain around your eyes & head.
- Eye redness: Red eyes caused by increased eye pressure.
- Colored halos around lights: Colored bright circles forming around light sources.
Any sudden onset of visual symptoms:
One should call an eye doctor immediately — including after hours. Sudden blurred vision in one or both eyes can sometimes indicate an underlying and potentially serious health problem such as stroke or diabetes.
When bacteria or viruses get into the space behind your nose, eyes, and cheeks, it causes sinusitis, or a sinus infection. These infections cause your sinuses to expand and mucus to build up in your nose. You'll feel pressure in the upper region of your face, especially behind your eyes and around your cheekbones.What are 5 signs of an eye injury? ›
- Eye pain. You should never ignore pain, especially if your eye has suffered trauma. ...
- Blurry vision. ...
- Burning feeling. ...
- Redness. ...
- Double vision. ...
- Droopy eyelid. ...
- Abnormal pupils. ...
- A sudden increase in floaters.
Eye trauma, foreign objects in the eye, chemical exposure to the eyes, and ocular infections are all considered eye emergencies and should be treated immediately. Seeking medical care as early as possible can help prevent permanent damage to your vision.What is blunt eye trauma? ›
A blunt eye injury is a type of injury in which you get hit hard in the eye, usually by an object such as a ball. A blunt eye injury may damage your eyelid, eyeball, and the thin bones behind your eyeball.What causes sudden vision impairment? ›
Common causes of sudden vision loss include eye trauma, blockage of blood flow to or from the retina (retinal artery occlusion or retinal vein occlusion), and pulling of the retina away from its usual position at the back of the eye (retinal detachment).
It might be brought on by eye strain, possibly because you've spent too much time in front of a computer or other screen. It can also be a sign of a refractive error, like nearsightedness (myopia) or farsightedness (hyperopia), which can be easily solved with a new eyeglasses prescription from your eye doctor.What are 3 very common vision problems? ›
Most people who start needing glasses or contacts while they're young have at least one of three common vision problems: myopia, hyperopia, and astigmatism. These are all refractive errors, which means they're problems with the way the eyes focus light, rather than an eye disease.What is the most common eye hazard? ›
Dust is probably the most basic, most common eye hazard that workers face. Especially if you work outdoors. Those who work in construction, mining, woodworking, and the oil and gas industries deal with dust hazards on a daily basis.What are the two most common eye injuries? ›
- Black eye: A blow to the eye or the tissue around it causes a black eye. ...
- Bleeding in the eye: An eye surface hemorrhage (bleeding) can result from straining too hard (such as during a cough) or from trauma to the eye.
- Central vision loss. The central part of the retina concentrates the cells responsible for visual acuity. ...
- Peripheral vision loss. In people with impaired peripheral vision, the visual field narrows. ...
- Blurry vision. ...
- Visual disorders following brain injuries.
- High blood pressure. ...
- Heart disease. ...
- Diabetes. ...
- Rheumatoid arthritis. ...
- Thyroid disorder. ...
- Parkinson's disease. ...
- Cancer. ...
- Multiple sclerosis.
The four most common eye conditions leading to loss of vision or blindness are: Cataracts. Diabetes-related retinopathy. Glaucoma.What is the 10 common hazard? ›
Some industries naturally carry more risks, but we have outlined the top 10 most common workplace hazards that pose a threat: Hazardous chemicals, which include the following: acids, caustic substances, disinfectants, glues, heavy metals (mercury, lead, aluminium), paint, pesticides, petroleum products, and solvents.What is the most common reason people get eye injuries? ›
The most common causes of eye traumas include: Direct impact: Getting hit in the eye with an object coming toward you at full force such as a ball or nerf gun bullet. Blunt force trauma: This occurs when a blunt object impacts the eye, most commonly as a result of a large ball, car accident or a punch to the eye.What are the 3 common refractive conditions of the eye? ›
- Nearsightedness (myopia) makes far-away objects look blurry.
- Farsightedness (hyperopia) makes nearby objects look blurry.
- Astigmatism can make far-away and nearby objects look blurry or distorted.
- Presbyopia makes it hard for middle-aged and older adults to see things up close.
- Optic Neuropathies. Damage to the optic nerves can cause pain and vision problems, most commonly in just one eye. ...
- Optic Neuritis. ...
- Giant Cell (Temporal) Arteritis. ...
- Chiasm Disorders.
scratches and abrasions – such as from fingernails or tree branches. foreign bodies – such as small pieces of grit, wood or metal getting in the eye. penetrating or cutting injuries – such as cuts from glass or projectiles flung from tools, especially when hammering or using power tools.What is hyphema of the eye? ›
Hyphema is the collection of blood in the anterior chamber of the eye. The most common cause of hyphema is blunt trauma, though spontaneous hyphemas can occur in the setting of sickle cell disease or other increased bleeding states.