236. Eye Disorders

Anatomy

Ethmoid sinus (lamina papyracea) is medial surface of orbit. Most likely sinus wall to break with blunt eye trauma. Look for subcutaneous emphysema.

Ophthalmic artery is first major branch of intracranial portion of internal carotid artery. Ophthalmic veins communicate with cavernous sinus which don’t have valves as well.

Conjunctiva: outermost layer, thin, transparent mucous membrane. Episclera is deep to conjunctiva; contains blood vessels. Sclera is collagenous protective coating of the eye.

Physical Exam

Visual Acuity: check with eyes corrected (glasses or contacts). If unavailable, get notecard with 18g pin-hole in it (only parallel light rays to fall on macula and estimates corrected vision).

Snellen chart: 20 feet away and acuity is measured as 20/? with denominator is distance with a normal person could see those same letters. Determined by smallest line someone can read with one half of the letters correct. Rosenbaum chart can be used as near card (14 in from the patient).

Optokinectic nystagmus: involuntary horizontal nystagmus that occurs to exclude blindness in otherwise normal exam. (iPhone App; Youtube)

Visual Fields: Check 4 quadrants. If lesion is on the same side (left or right) on each eye, lesion is proximal to the optical chiasm. Bitemporal hemianopia can occur in pituitary adenoma.

Mobility: Extraocular muscles innervated by CNIII, CNIV, and VI. IV (Trochlear): innervates superiof obliquie – pulls toward the nose (inferomedially). VI (Abducens): innervates lateral rectus – pulls eye laterally. All others innervated by III (oculomotor). Diplopia is usually worse when looking in same direction as malfunctioning muscle. Monocular diplopia is usually a lens or corneal irregularity (or just malingering).

Pupils: APD (afferent pupillary defect, Marcus-Gunn pupil) usually indicated optic nerve problem. Swinging flashlight test – shine light on pupil, then shine light on opposite pupil. The opposite pupil will dilate because light is not getting thru to the CNS. Can also occur with severe vitreous hemorrhage, retinal pathology. (Youtube)

Hypopyon: WBCs in the anterior chamber. Hyphema: RBCs in the anterior chamber. Flare: headlights in the fog. Usually caused by increased protein in the chamber, usually due to inflammation (iritis).

Seidel test: streaming of fluorescein-tinged aqueous humor seen in full thickness laceration of cornea. Can be negative with small or spontaneously sealed corneal laceration.

Intraocular Pressures: Do not measure if concerned about globe rupture. Normal pressure 10-20mmHg.

Ocular Infections

Preseptal Cellulitis: infection of eyelids and periocular tisues anterior to orbital septum. Associated with URIs, paranasal sinusitis. Staph aureus, staph epidermidis, strep. Full painless ocular motility is intact. Nontoxic pts can be treated with Augmentin or Keflex, though consider in more severe cases MRSA/3rd generation cephalosporins.

Postseptal or Orbital Cellulitis: usually due to paranasal sinusitis. S. aureus, strep pneumoniae, and anaerobes MCC. Pain with moving the eyes. If muscles involved, consider cavernous sinus thrombosis. Requires hospitalization and IV abx (Unasyn, carbapenems, 3rd gen cephalosporins). Consider lateral canthotomy if IOPs are elevated. Complications include CVT, osteomyelitis, empyema, meningitis.

Stye: external hordeolum – folliculitis on eyelid (usually staph). Located on lash line and looks like pimple. Tx: warm compresses and erythromycin ointment x 1 week.

Chalazion: acute/chronic inflammation of eyelid secondary to blocked duct. Painless lump. Tx is the same as stye. Hard to differente chalazion from internal hordeolum.

Blepharitis: eyelash follicle inflammation. Overgrowth of staph epidermitis. Tx usually just cleaning in the morning, sometimes requires abx drop/ointment.

Conjunctivitis: usually viral which is benign, self-limited. Bacterial: unilateral, though can be bilateral, mucopurulent discharge adherence of eyelids in the morning. Preauricular lymphadenopathy absent. Usually staph/strep. Need to do fluorescein staining to look for ulcer/abrasion/dendrite. Tx: topical abx 4x daily x 1 week. Polytrim fine, cipro/ofloxacin for contact wearers. Viral: adenovirus (pink eye): preceded by URI, watery discharge. Usually both eyes over the course of a few days. Preauricular adenopathy present. Look for follicles on inferior palpebral conjunctiva.Conjunctival Follicles

Tx with ocular decongestant (Naphcon-A) one drop TID with cool compresses and artificial tears – can take 1-3 weeks. Allergic conjunctivitis: itching, similiar to viral. Tx: cool compresses 4x daily, topical antihistamine/decongestant.

Herpes Zoster Ophthalmicus: shingles of first division of trigeminal nerve. Involves upper eyelid. Can involve tip of nose as well (Hutchinson sign). Cornea will have pseudodendrite where as HSV will have dendrite (stains better).Dendrite

Tx: With skin involvement, tx with oral antiviral fo 7-10d. Ayclovir 800mg 5x daily, famciclovir 500mg TID or Valacyclovir 1g TID. Tx corneal involvement with bacterial ointment to prevent bacterial secondary infection.

Corneal Ulcer: serious infection involving multiple layers of cornea. Caused by desquamation, trauma or direct microbial invasion. Pseudomonas can be culprit in contact wearers. Exam reveals white, hazy base ulcer. Tx: close f/u with ophtho, fluoroquinoline (Cipro or ofloxacin) drops qhr. Do not patch the eye. Complications including scarring, perforation, glaucoma, cataracts.

Uveitis/Iritis: anterior chamber inflammation. Conjunctival injection, photophobia, decreased vision. No drainage. Perilimbal flushing (injection greatest around limbus). Consensual photophobia (pain with light shine on unaffected eye). Pupil usually miotic poorly reactive. Flare and cells in anterior chamber. Tx: blocking pupillary sphincter and ciliary body with long acting cyclopegic agent (homatropine for 2-4 days and tropicamide with decrease pain. Need to see ophtho in 1-2 days.

Endopththalmitis: inflammation of aqueous or vitreous humor that can lead to loss of vision. Most frequent cause is postsurgical followed by penetrating ocular trauma. Erythema and swelling of eyelids, sclera injection, chemosis, hypopyon, and uveitis. Tx emergent intravitreal abx and steroids + systemic abx.

Vitreous Hemorrhage: sudden painless vision loss, sudden black spots/cob webs/haziness. Can be caused by diabetic retinopathy, posterior vitreous detachement in elderly, ocular trauma in shaken baby. Consider retinal detachment.

Subconjunctival Hemorrhage: rupture from trauma, increased venous pressure related to valsalva, spontaneous as well. Exam normal outside of hemorrhage. Resolves in 2 weeks spontaneously. Bloody chemosis is raised, bullous appearance.

Conjunctival Abrasion/Laceration: conjunctiva not innervated as much as cornea so not as painful. Rule out globe rupture with Seidel test (fluorescein should not flow out of laceration) though rupture can still occur if small or already closed.

Corneal Abrasion: highly innervated so can be extremely painful. Foreign body sensation, photophobia, tearing. Relief to pain with topical anesthesia is virtually diagnostic for abrasion. Iritis can occur if abrasion large or > 24 hours since injury. If there are several linear abrasions, consider looking for FB still stuck in the eyelid. Tx: cycloplegics (cyclopentolate 1% or homatropine 5% one drop q6-8hrs) relive some of the spasm and decrease secondary iritis. Topical NSAIDs like ketorolac and diclofenac give some relief and dont decrease healing time. Some recommend against giving topical anethetics to go home with.

Corneal Laceration: full thickness can have mishappen iris. Small lacerations though appear very similiar to abrasions and can close spontaneously and be Seidel test negative. Consider CT orbit with id globe anatomy, contour, FB. Sensitivity to detection occult globe perforation is 56-68%. Can convert to endophthalmitis or traumatic cataract.

UV Keratitis: ‘snow blindness,’ ‘welder’s flash,’ exposure to UV light and eyes aren’t protected (welders, suntanners). Symptoms can develop after delay of 12 hours. FB sensation, photophobia. Diffuse punctate corneal edema, punctate corneal abrasions. Tx: cycloplegics, topical abx, double patching of both eyes if pt requests, healing in 24-36 hrs.

Corneal FB: Metal sitting for several hours will form ‘rust rings’ – if longer than 24 hours, can get iritis. Presence of hyphema suggests globe perforation. Seidel test will be positive. Removal: Irrigate with NS first and see if very superficial FB will be irrigated off. Next, try moistened cotton applicator. Full thickness corneal FB should be removed by opthalmologist. Otherwise, 25g needle or sterile FB spud on Alger brush. Rust ring can be cleared by spur, but very often rust forms again the following day which can be toxic to the eye so will need to be seen by optho again the following day, but rust ring do not need to be removed in the ED. Tx: topical abx, cycloplegics, tetanus if needed, f/u with optho next day.

Lid Lacerations: Lacerations involving lid margins, within 6-8mm of medial canthus, involving lacrimal duct/sac, involving inner surface of lid, wounds associated with ptosis, those involving tarsal plate or levator palpebrae muscle (orbital fat present) need specialist repair. Can instill flourescein into eye and see if it appears in the wound to assess for canalicular involvement. Can sometimes be discharged if repair will occur the following day. Small lacerations <1mm at the lid edge do not need sutures and can heal spontaneously. Any laceration > 1mm at the lid edge needs repair by specialist.

Hyphema: blood in anterior chamber. Traumatic or spontaneous (sickle cell). Tx: Elevate head, dilate pupil (prevents further bleeding). Consider lowering IOPs with B-blocker, IV mannitol, topical a-adrenergic agonist (apraclonidine), or oral/topical/IV carbonic anhydrase inhibitors (CAIs) – do not give to sickle cells – will lower pH causing sickling increase risk for clogging ie increased IOP. Rebleeding occurs in 3-5 days. Consider admittting hyphema vs very close followup. If hyphema less than 1/3, can discharge.

Blow-out Fractures: MC site is inferior wall (maxillary sinus, entraps inferior rectus muscle causing restriction of upward gaze and diplopia) and medial wall (ethmoid sinus thru lamina papyracea, subcutaneous emphysema). Isolated blow-out fractures with/out entrapment do not require immediate surgery for repair within 3-10 days. Waters view xray shows cloud maxillary sinus for entrapment. Oral abx recommended. All blow out fractures should be referred for dilated eye exam to rule out retinal tear/detachment.

Ruptured Globe: Can be penetrating or blunt (impact on orbital rim can cause increased IOP to the point of rupture). Look for tear-drop or irregular shaped pupil, AFD, shallow anterior chamber, hyphema, positive Seidel test, lens dislocation. IOPs should not be measured due to possibility of extruding introcular contents. CT orbits to look for FB. If suspected, elevated head, protective metal eye shield, broad spectrum IV, tetanus. Likely need emergent surgery.

Retrobulbar Hematoma: due to blunt trauma. If large, can increase IOP, decrease blood flow to optic nerve and vision loss. Causes proptosis, pain, decreased vision. CT will show hemorrhage. IOP > 40mmHg – needs emergent canthotomy.

Lateral canthotomy: C/I: luxated globe (eyelids not visible) – need to have eye reduced. Equipment: hemostat, suture scissors, pickups, lidocaine with epi.

Numb the lateral portion of the eyelid, your going to crimp it with hemostat to reduce capillary blood flow. Then cut (extend) the skin until you see the inferior ligament and cut that. That usually does it, but you can cut the superior ligament as well. Afterward, IOP decreases, APD resolves, visual acuity improves. Ophthalmologist really doesn’t do anything afterward. Doesn’t need to ‘re-attach’ the ligament or cosmetically fix the previous incisions. Usually heals well afterward.

Chemical Ocular Injury: complications include scarring causing vision loss. Use NS irrigation. Alkali injuries more common than acid. Ammonia and lye found in household cleaners, drain cleaners. Alkali are more serious than acid due to causing liquefaction necrosis (deep penetration into liquids). Acid causes coagulation necrosis preventing deep penetration. Tx: instill topical anesthetic first, then irrigation for 30 minutes. Check pH and continue if pH > 7.4. Irrigation with NS or other isotonic solution via eye irrigating solution via Morgan lens. Usually causes conjunctival injection and chemosis, though severe can cause scleral whitening. Alkaline substances with pH < 12 or >2 should not cause serious injury. If corneal clouding or epithelial defect, should receive prompt optho referral.

Cyanoacrylate: superglue. Rarely permanent damage. Place large amounts of erythromycin ointment on the eye and it should clump together. Do not need to have all of it removed at once. Can have rest removed next day.

Acute Angle-closure Glaucoma: increased IOP due to outflow obstruction. Occurs suddenly usually when pupil dilates (usually the trigger – parasympatholytics, sympathomimetics, dim illumination, emotion upsetting events, causing cornea closure. Cornea becomes edematous and less transparent – foggy vision or halos. Cloudy, dilated eye – conjunctiva injection. Cataracts, farsighted increases risk of acute angle glaucoma. Sudden onset, painful, significant vision loss. Nausea/vomiting as well. Fixed, mid-position pupil and hazy cornea with conjunctival injection at limbus. Eye is rock hard. Normal IOP 10-20, can exceed 60-80 in acute attack. Tx: lowering production of aqueous humor: (topical B-blocker timolol), alpha-adrenergic agonists (apraclonidine) and CAIs (acetazoleamide); faciliting outflow humor (parasympathomimetic miotic agents – pilocarpine); reducing humor volume (mannitol). IV mannitol quickly lowers IOP and should be given if no contraindications. Definitive tx is laser iridectomy.

Optic Neuritis: idiopathic or MS. acute onset of vision loss. Not very painful, but can be painful with eye movements. Vision loss occurs over days, sometimes over hours. Usually unilateral. Color vision affected more than complete vision – red desaturation. APD common as well. Will have swollen/edematous optic disk (papillitis). Tx: consult neurology – ONTT trial supported IV steroids, not oral steroids.

Central Retinal Artery Occlusion: first branch off internal carotid artery is ophthalmic artery – if occluded, inner retina infarcts – causing pale, less transparent, edematous retina. macula still present – looks like cherry red spot. Sudden (over seconds) painless monocular loss of vision – preceded by amaurosis fugax. Exam has APD, pale retina (yellow/white), cherry red macula, box-carring (cattle-trucking) of arterioles. Non-evidence tx with digital massage, IOP lowering drugs, breathing into bag to increase PaCO2. No exact treatment placed at this time. HBO can be an option.

Central Retinal Vein Occlusion: CRAO. Sudden painless vision loss. Occlusion of retinal vein causes stasis, edema and hemorrhage. Loss of vision varies. RF: DM, HTN, CVA, CV, hypercoaguable, vasculitis, no idea. Diffuse retinal hemorrhages in all 4 quadrants – ‘blood and thunder’ fundus. No specific tx. Consult neuro/optho.

Flashing Lights/Floaters/Retinal Detachment: Always unilateral (bilateral usually means intracranial process such as opthalmic migraine). Vitreous gel shrinks over time causing it to separate from posterior wall. Average age of onset if 55yo. If gel separates successfully, floaters occur. If pull causes tear in retina, fluid can disperse into space and peel retina off called retinal detachement – dark veil or curtain in the field of vision. Most tears occur in peripheral retina. If tear involves macula, repair should occur within a few days. If not, should occur with 10 days. Ophtho consult for dilated indirect exam within 24 hours.

Giant Cell Arteritis: temporal arteritis. systemic artertitis involving medium sized arteries in carotid circulation. causes painless ischemic optic neuropathy. Generally >50yo, hx/o polymyalgia rheumatica. Headache, jaw claudication, fatigue, fever, anorexia, temporal artery tenderness. 1/3 have stroke symptoms. Severe vision loss with contralateral side involved if not treated. APD present. ESR usually range 70-110. Tx: IV steroids f/u by oral steroids. Biopsy will be positive for a week after starting therapy.

Bell’s Palsy: cranial nerve VII palsy. Usually viral in origin. Ipsalateral upper and lower face – orbicular muscles involved – incomplete closure of eyelids. Need eyedrops to prevent keratitis. Tx always changing over steroids vs antivirals + steroids. Check extraocular movements – Genu VII Bell’s palsy is stroke involving CNVI + CNVII – will have paralysis of abduct of ipsalateral eye (CNVI palsy).

CNIII palsy: diabetic related usually with pupil spared. Unable to medial gaze, upward gaze and downward gaze as well as some ptosis. Lateral gaze will be preserved. diplopia worse with pt looking to contralateral side. If ipsalateral pupillary dilation noted, it is a posterior communicating artery aneurysm until proven otherwise.

CNVI palsy: (Abducens) Lateral gaze will be diminished. Need to check for intracranial lesion.

Horner’s syndrome: ipsalateral ptosis (drooping eyelid), miosis (pinpoint pupil), anhydrosis (no sweating). blocked sympathetic nerve. Recommend looking for possible blockage along path – CXR, CT brain/cervical region, CTA head/neck for carotid dissection. Causes: CVA, tumor, dissection, zoster, trauma in adults. In kids, neuroblastoma, lyphoma, metastasis.

Papilledema: bilateral edema of head of optic nerve due to increased ICP. Causes: malignant HTN, pseudotumor cerebri, intracranial tumors, hydrocephalus. Papillitis is unilateral, papilledema is bilateral. Optic disk is blurred, cup is diminished/absent, flamed shaped hemorrhages seen near nerve heard. Prolonged preservation of visual acuity (asymptomatic frequently).

Optic Nerve Sheath Diameter

Do ocular ultrasound with linear probe. Check the diameter of the dense black optic nerve 3mm posterior to the eye.

In an adult, normal ICP is under 5mm. Anything above this correlates with elevated ICP.

Crescent Sign: Echolucent circle within the optic nerve in severely elevated ICP.

Mount Sinai: Optic Nerve Papilledema and Crescent Sign

Sometimes optic nerve sheath can appear dilated with normal ICP. Do the 30 degree test.

30 degree test: check diameter with patient looking straight and then check it again with patient looking 30 degrees in another direction. If increased diameter due to increased ICP, the optic nerve stretches with the change in gaze and the diameter should be lower. If the diameter does not change, likely due to parenchymal infiltration or thickening of the optic nerve. (Emergency Ultrasound, Matthew Lyon and Michael Blaivas, 2008)

Optic Nerve ultrasound for the detection of raised ICP, 2011: Checked optic nerve diameter on neuro ICU patients with EVDs in place to measure their ICP. Noted sensitivity of 96% when using diameter of > 4.8mm.

Pseudotumor Cerebri (Idiopathic Intracranial Hypertension): Increased ICP, papilledema nd normal CXR and normal CT/MRI. Nausea/vomiting/headaches/blurry vision. Can causes CNVI palsy causing horizontal diplopia. Basically need LP – Tx: acetazolamide 500mg PO BID + neurology consult.

Questions

Q. Which eye drop for acute angle glaucoma is NOT used to decrease aqueous humor production? A. Pilocarpine – used to faciliate outflow. Timolol, apraclonidine, and acetazolamide are used to decrease production.

Resources

Tintinalli, Seventh Edition, Chapter 236: Eye Emergencies

2 PK’s: Preemie Delivery / Central Retinal Artery Occlusion, Davut Savaser, eMedHome, AAEM Scientific Assembly 2016

236. Eye Disorders

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