CDUPA26- Ophthalmology Part 2 (maya)

What is Preseptal (Periorbital) Cellulitis?

Inflammation and infection of the eyelid and soft tissues that are anterior and superficial to the orbital septum.

What are common causes of Preseptal Cellulitis?

Usually occurs secondary to a superficial skin infection arising within or near the eyelid itself (e.g., hordeolum, recent lid surgery, or a traumatic wound/bite).

What are the most common pathogens causing Preseptal Cellulitis?

Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae.

What are the clinical manifestations of Preseptal Cellulitis?

More common in children, unilateral eyelid swelling, erythema, and pain, with the eyeball remaining unaffected.

What symptoms are notably absent in Preseptal Cellulitis?

No limitation of extraocular movements (EOM), no proptosis, and no chemosis. The patient generally should not have a fever.

How can you differentiate Preseptal Cellulitis from Dacryocystitis?

Preseptal cellulitis involves swelling of the entire eyelid area, not just the lacrimal sac, and there is a lack of purulent discharge on palpation of the puncta in preseptal cellulitis.

What is the preferred diagnostic imaging for Preseptal Cellulitis if the diagnosis is unclear?

A CT scan of the orbits.

What is the management for Preseptal Cellulitis?

Outpatient, empiric antibiotic therapy for 5-7 days with oral antibiotics such as Amoxicillin-clavulanic acid (Augmentin). Hospitalization with IV antibiotics may be necessary if the patient is under 1 year old or severely ill.

What is Orbital Cellulitis, and why is it a medical emergency?

Orbital cellulitis is a serious infection involving the ocular muscles and fat within the orbit. It can be sight- and life-threatening and requires emergency attention.

What are the risk factors for developing Orbital Cellulitis?

Predisposing factors include dental or sinus infections, particularly rhinosinusitis (~80% of cases).

What are the most common pathogens causing Orbital Cellulitis?

Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and some gram-negative bacteria.

What are the clinical manifestations of Orbital Cellulitis?

Fever (unlike preseptal cellulitis), unilateral ocular pain, eyelid swelling, erythema, proptosis, chemosis, purulent discharge, sluggish pupillary response, ophthalmoplegia, impaired EOM, and pain with eye movement due to inflammation.

What diagnostic tests are used for Orbital Cellulitis?

Cultures of the orbit (if surgical drainage is performed), nose/sinus, and blood. A CBC will typically show leukocytosis (elevated white blood cell count), and imaging such as a CT scan of the orbit and sinuses may be needed.

What is the management for Orbital Cellulitis?

Patients need to be admitted. Management includes ENT and ophthalmology consultation, starting empiric IV antibiotics (Vancomycin plus 3rd-generation cephalosporin or beta-lactamase resistant drug like piperacillin-tazobactam). Surgery may be indicated if there is no response to antibiotics or if an abscess is identified. Once the patient is improving and afebrile, oral antibiotics are continued for 2-3 weeks.

What are key imaging findings in Orbital Cellulitis on a CT scan

The CT scan may show proptosis, orbital fat stranding, and other signs of orbital involvement.

Why is visual acuity considered a vital sign when dealing with eye concerns?

Visual acuity is important because it can help assess eye function before swelling or other complications make evaluation more difficult.

When should visual acuity be assessed in a patient with eye trauma?

Visual acuity should be checked first before conducting any other examination, especially in cases of traumatic eye injuries where swelling might worsen during the exam.

What are the typical causes of an orbital blowout fracture?

It usually occurs due to trauma such as being punched in the face, motor vehicle accidents (MVAs), or being hit in the eye by objects like a baseball.

What are the most common clinical manifestations of an orbital blowout fracture?

Clinical manifestations include diplopia (due to entrapment of inferior rectus muscle), impaired or restricted extraocular movements (EOM), pain with EOM, periorbital ecchymosis (bruising), subcutaneous orbital emphysema, enophthalmos (sunken eye), exophthalmos (bulging eye), or orbital dystopia, and facial numbness (due to damage to the trigeminal nerve's maxillary zone).

What diagnostic imaging is typically used for an orbital blowout fracture?

A CT scan of the orbit is used to assess the fracture and potential complications.

What are potential complications of an orbital blowout fracture?

Potential complications include brain injury, infection, orbital compartment syndrome (high intraocular pressure), and ruptured globe.

What is the management for an orbital blowout fracture?

Management includes an urgent surgical consult (maxillofacial, plastic, or ENT surgeon), ophthalmology consult (for evaluating visual acuity and potential eye dysfunction), prophylactic oral antibiotics (e.g., Augmentin), cold compresses, corticosteroids (to reduce swelling and help with diplopia), and patient education to avoid blowing the nose or sneezing (to prevent worsening of orbital emphysema).

What are some common types of foreign bodies found in the eye?

Foreign bodies can include metal, glass, organic material, and they can be found either on the surface of the cornea or penetrating into the globe (which is more concerning).

Why is the history of an ocular foreign body important?

History provides details about occupation, recent activities, recent trauma, and the use of protective goggles, all of which are important for evaluating the risk and cause of a foreign body in the eye.

What are the clinical manifestations of an ocular foreign body?

Clinical manifestations include foreign body sensation, eye pain or irritation, conjunctival injection, ciliary injection, and rust rings in cases of metal foreign bodies.

What diagnostic tools are used to identify an ocular foreign body?

Diagnosis involves a flipped lid exam to locate the foreign body and a slit lamp exam with fluorescein staining to identify corneal abrasions or foreign bodies.

What is the management for an ocular foreign body?

Management includes removing the foreign body with anesthetic application (using irrigation, cotton swab, or needle if experienced), referring to ophthalmology for rust ring removal or in cases of suspected globe injury, providing pain relief with oral NSAIDs or topical drops, and administering topical antibiotics to prevent superinfection.

What is a corneal abrasion and what typically causes it?

A corneal abrasion is the most common eye injury caused by minor trauma such as a small foreign body, contact lens, or fingernail.

What are the clinical manifestations of a corneal abrasion?

Significant eye pain, irritation, foreign body sensation, and photophobia are common due to the dense corneal innervation by the trigeminal nerve. Vision impairment may also occur if the abrasion is large or overlaps the visual field.

What is the diagnostic approach for a suspected corneal abrasion?

Diagnosis includes checking visual acuity, evaluating for retained foreign bodies (using a flipped lid exam), and performing a slit lamp exam with fluorescein to identify epithelial defects.

What is the management for a corneal abrasion?

Management includes saline irrigation, topical antibiotics (ointment preferred), pain relief (oral NSAIDs or cycloplegics), and patching the eye for large abrasions (>10 mm) for no more than 24 hours. Ophthalmology follow-up is needed for large abrasions, and oral opioids may be prescribed if necessary.

What causes a ruptured globe or penetrating globe injury?

It occurs secondary to high-velocity projectiles, high-impact blunt trauma, or sharp object injuries.

What are the clinical manifestations of a ruptured globe?

Markedly decreased visual acuity, relative afferent pupillary defect, teardrop pupil, external prolapse of the uvea or ocular structures, tenting of the cornea or sclera, Seidel sign (fluid leaking), and subconjunctival hemorrhage or hyphema.

What should be avoided in the treatment of a ruptured globe?

Avoid any procedure that increases pressure on the eye, such as tonometry or everted eyelids, and avoid administering medication into the eye unless by an eye specialist.

What diagnostic imaging is used in suspected ruptured globe cases?

CT scan of the orbit to rule out associated fracture and retained foreign body.

How is a ruptured globe managed?

Management includes rigid eye shield placement, bed rest (NPO—nothing by mouth bc pt. will need surgery), antiemetics, pain medication (excluding NSAIDs), emergent ophthalmology consult, empiric antibiotics (vancomycin and ceftazidime), and surgical globe repair.

What are complications associated with a ruptured globe?

Loss of vision and endophthalmitis (internal eye infection).

What is hyphema?

Blood in the anterior chamber of the eye, usually resulting from blunt or penetrating eye injury.

What are the clinical manifestations of hyphema?

Vision loss, eye pain, nausea, vomiting, photophobia, and elevated intraocular pressure (IOP).

How is hyphema managed?

Elevate the head of the bed to 30 degrees, bed rest, dim lighting, pain and nausea control, and ophthalmology consult. In severe cases, clot evacuation may be needed.

What is the grading system for hyphema based on?

The percentage of the anterior chamber filled with circulating red blood cells, with Grade I being less than 33%, and Grade IV being a completely filled chamber.

Why are chemical injuries considered an ophthalmologic emergency?

They can result in permanent vision loss.

Why do alkaline substances cause more severe chemical injuries than acidic substances?

Alkaline substances cause saponification, leading to deeper tissue penetration and necrosis, while acids cause more superficial coagulation necrosis.

What are the clinical manifestations of a chemical eye injury?

Moderate-to-severe eye pain, decreased vision, blepharospasm, conjunctival redness, and photophobia.

How is a chemical eye injury managed?

Continuous irrigation with water or saline until the pH is neutral, avoiding any use of a Morgan Lens if a globe injury is suspected, and initiating antibiotic drops or ointment once irrigation is complete.

When should the Morgan Lens be used in chemical eye injury management?

After irrigation flow is started, with proper insertion under the eyelid.

What is diabetic retinopathy, and who is most at risk?

Diabetic retinopathy is a microvascular complication of diabetes, the leading cause of preventable blindness in adults aged 25-74, particularly more common in Black, Latino, and Asian populations.

What are the two types of diabetic retinopathy?

Proliferative and nonproliferative retinopathy.

What are the risk factors for developing diabetic retinopathy?

Duration of diabetes and level of glycemic control.

What are the clinical manifestations of diabetic retinopathy?

Blurry vision, diplopia, narrowing of the visual field, dark spots, floaters, discomfort in the eyes, difficulty seeing in dim lighting.

How can the progression of diabetic retinopathy be slowed?

Maintaining HbA1c below 7%, managing blood pressure and hyperlipidemia, and undergoing regular eye exams.

What are the American Diabetes Association's recommendations for screening for diabetic retinopathy?

Patients with Type 1 diabetes should have their first fundoscopic exam within 5 years of diagnosis, and patients with Type 2 diabetes should have the exam at the time of diagnosis. If no retinopathy is found, exams should be repeated every 1-2 years; if present, exams should be repeated at least annually.

What is seen on a fundoscopic exam in nonproliferative diabetic retinopathy (NPDR)?

Cotton wool spots (affected nerve fibers), intraretinal hemorrhages, hard exudates, microvascular abnormalities (microaneurysms, occluded vessels, dilated vessels), and no neovascularization.

How is nonproliferative diabetic retinopathy managed?

Management includes adequate glycemic, blood pressure, and lipid control, ophthalmology referral for anti-VEGF injections (e.g., ranibizumab, bevacizumab), laser therapy, intravitreal steroids, and possibly vitrectomy.

What differentiates proliferative diabetic retinopathy from NPDR in a physical exam?

Neovascularization from the optic disc or retinal vessels is seen in PDR.

What is the risk of vision loss in proliferative diabetic retinopathy?

Vision loss can occur abruptly if the neovascularization leads to bleeding that obstructs light from reaching the retina.

How is proliferative diabetic retinopathy managed?

Combination therapy with panretinal photocoagulation and anti-VEGF agents, laser therapy, intravitreal steroids if macular edema is present, and pars plana vitrectomy for progressive disease.

What causes hypertensive retinopathy?

Hypertensive retinopathy is caused by vasoconstriction, arteriosclerosis, and increased vascular permeability due to hypertension, which leads to breakdown of the inner blood-retinal barrier.

What are the clinical manifestations of hypertensive retinopathy?

It is usually asymptomatic until late in the disease course, but patients may experience cloudy vision, diplopia, headaches, and eventual vision loss.

What are the fundoscopic findings in hypertensive retinopathy?

Findings include arterial vasoconstriction, arteriosclerosis (copper wiring), arteriovenous (AV) nicking, focal axonal swelling (cotton wool spots), and exudation (macular star).

How is hypertensive retinopathy managed?

Management includes controlling high blood pressure, using anti-hypertensives, and intervening in malignant hypertension (>180/120 mmHg) with IV medications such as nicardipine, sodium nitroprusside, or labetalol.

What is macular degeneration, and what are the two types?

Macular degeneration is a progressive eye condition that affects the central portion of the retina, leading to vision loss. It can be classified as "wet" or "dry."

What are the risk factors for macular degeneration?

Risk factors include family history, increasing age, white race, female gender, smoking, and certain drugs like chloroquine or phenothiazine.

What are the clinical manifestations of macular degeneration?

Patients experience metamorphopsia (visual distortion), scotomas (blind spots), and loss of central vision.

What is seen on a retinal exam in dry macular degeneration?

Accumulation of drusen beneath the retina, atrophy of the retinal pigment epithelium, and pigment clumping are seen.

How is dry macular degeneration managed?

There is no specific treatment, but progression can be slowed with oral vitamins (C, E, antioxidants, zinc, copper) and tobacco cessation.

What is seen on a retinal exam in wet macular degeneration?

Large soft drusen and new blood vessels (neovascularization) beneath the retina are seen, which may leak blood and fluid.

How is wet macular degeneration treated?

Treatment includes stopping angiogenesis through laser photocoagulation, photodynamic therapy, and intravitreal anti-VEGF injections.

What is retinal detachment, and why is it an emergency?

Retinal detachment occurs when the retina separates from the retinal pigmented epithelium (RPE), most commonly due to posterior vitreous detachment. It is an ophthalmologic emergency.

What are the common causes of retinal detachment?

Retinal detachment can occur spontaneously or secondary to myopia, trauma, or inflammatory changes within the eye.

What are the clinical manifestations of retinal detachment?

Sudden onset of painless blurred or blacked-out vision, preceded by floaters ("cobwebs") or photopsia (flashes of light). Physical exam may reveal an afferent pupillary defect, and a fundoscopic exam demonstrates ridges of displaced retina flapping in the vitreous humor.

What is the management for retinal detachment?

Immediate referral to ophthalmology within 24 hours for laser, cryosurgery, or scleral buckle procedures. The patient should remain supine with the head turned to the side of the detachment.

What is amaurosis fugax?

Amaurosis fugax is transient loss of vision, which can be monocular or binocular. It is often associated with transient ischemic attacks (TIA) or stroke but can also occur with other disorders.

What should the evaluation of amaurosis fugax include?

A thorough history and physical exam, assessing stroke risk factors, and physical exam findings suggestive of etiologies. Diagnostic studies, such as a carotid doppler, may be performed based on likely causes.

What is CRAO, and why is it an emergency?

CRAO occurs when an embolus or thrombus causes blockage within the retinal artery, leading to retinal ischemia or infarction ("eye stroke"). It is an ophthalmologic emergency.

What are the common risk factors for CRAO?

Risk factors include carotid artery disease, hypertension, atrial fibrillation, valvular disease, diabetes mellitus, hypercholesterolemia, tobacco use, and a history of TIA or cerebrovascular accidents (CVA).

What are the clinical manifestations of CRAO?

Sudden painless loss of vision in one eye, often beginning in the upper field, and a curtain coming down over the eye. A relative afferent pupillary defect may also be present.

How is CRAO diagnosed?

A fundoscopic exam reveals a cherry red spot on the macula, retinal opacity, possible visible embolus, and box-car-ing of vessels. Fluorescein angiography may be performed if the diagnosis is unclear.

What is the management for CRAO?

Immediate management (within 24 hours) involves laying the patient supine, ocular massage, administering oxygen, and using IV acetazolamide. Hyperbaric oxygen therapy and medications may also be used. Surgical intervention for carotid artery stenosis may be needed in significant cases.

What is CRVO, and what causes it?

CRVO is caused by a blockage of a vein that carries blood away from the retina, typically due to a clot or arteriosclerosis. It results in hemorrhage, leakage of fluid, and eventual edema.

What are the clinical manifestations of CRVO?

Sudden painless monocular vision loss, scotomas, and blurry or distorted central vision due to macular edema. Transient visual obscurations may occur due to wax and wane symptoms. If severe, it can lead to retinal detachment and glaucoma.

How is CRVO diagnosed?

A fundoscopic exam reveals a "blood and thunder" appearance with retinal hemorrhages, edema, dilated retinal veins, and cotton wool spots. Visual acuity may be impaired, and fluorescein angiography can assess nonperfusion of the retina.

What is the management for CRVO?

Management includes regular ophthalmology follow-up, panretinal photocoagulation therapy for retinal neovascularization, and anti-VEGF injections for macular edema. Intravitreal steroids may also be used as an alternative.

What is the prognosis for CRVO?

Prognosis is better if baseline acuity is 20/60 or better, but worse if neovascularization or glaucoma is present. Branch retinal vein occlusion (BRVO) has a better prognosis than CRVO.

What causes Horner syndrome?

It occurs when there is a disruption to the sympathetic nerve fibers to the eye, which can occur at the spine, brainstem, or carotid artery. It can also be associated with lung cancer (Pancoast tumor).

What are the classic symptoms of Horner syndrome?

Miosis (pinpoint pupil), anhidrosis (lack of sweating), and ptosis (eyelid drooping), also known as the "MAP" triad.

What is the management for Horner syndrome?

Treatment involves managing the underlying cause.

What is optic neuritis, and what conditions is it associated with?

Optic neuritis is the acute inflammatory demyelination of the optic nerve. It is commonly associated with multiple sclerosis (MS) and neuromyelitis optica (NMO).

What are the clinical manifestations of optic neuritis?

Acute unilateral loss of vision, central scotoma, pain with eye movement (EOM), loss of color vision, photopsia, and a relative afferent pupillary defect (Marcus Gunn pupil).

How is optic neuritis diagnosed?

Diagnosis is made with the swinging flashlight test, fundoscopic exam (showing optic disc swelling or blurred disk), and an MRI with gadolinium contrast to work up MS.

What is the treatment for optic neuritis?

IV steroids (1 g methylprednisolone IV for 5 days) are the primary treatment. Vision will take weeks to improve if left untreated, and there is a 35% recurrence rate.

What is papilledema, and what causes it?

Papilledema is optic disc swelling due to elevated intracranial pressure. Causes include hypertensive emergencies, idiopathic intracranial hypertension (pseudotumor cerebri), brain lesions, hemorrhagic stroke, and increased cerebrospinal fluid.

How is papilledema diagnosed?

It is diagnosed through a fundoscopic exam, which shows a swollen and enlarged optic disc, and imaging such as MRI with contrast and lumbar puncture (if appropriate).

What is the management for papilledema?

Treat the underlying cause.

What is nystagmus, and what are its phases?

Nystagmus is rhythmic oscillation of the eyes, with a slow phase of drift in one direction and a fast phase of corrective quick jerk in the opposite direction.

What are the clinical manifestations of nystagmus?

It can affect balance and coordination, and patients may have vertigo or difficulty fixating on one object. Nystagmus can be vertical, horizontal, or rotary/torsional.

What are the conditions in which nystagmus is seen?

It is seen in vestibular conditions such as vestibular neuritis, BPPV, albinism, and neurological conditions like stroke, tumors, and multiple sclerosis (MS).

How is nystagmus diagnosed and managed?

Diagnosis depends on patient risk factors and associated signs. For vestibular neuritis, a HINTS exam may be performed; for BPPV, Dix-Hallpike maneuvers are helpful. Imaging may be used if stroke is suspected. Management focuses on treating the underlying condition.

You are evaluating a patient in the emergency department who presents with chief complaint of "cellulitis around the eye". You immediately become concerned that you may be dealing with life and vision threatening illness. All of the following findings would be more concerning for orbital cellulitis over preseptal cellulitis except:

A. Eyelid swelling

When comparing and contrasting periorbital cellulitis compared to orbital cellulitis, it's important to recognize which symptoms/findings are associated with both conditions and which is only associated with orbital cellulitis. This is imperative because orbital cellulitis is life and vision threatening while preseptal cellulitis is not.

A 31-year-old man presents to the emergency department after getting hit in the face with a baseball. He is reporting right eye and facial pain as well as double vision. Vital signs are within normal range. Visual acuity is obtained: OD 20/100, OS 20/20, OU 20/60. On physical examination, the patient cannot look up with the right eye. The eye appears sunken in and swollen. Sensation over the right cheek is reduced. What diagnostic study would be most helpful at this time to further evaluate the patient's suspected condition?

B. CT scan of the face and orbits

This is a second order question, which means we first had to identify the suspected diagnosis (orbital blow out fracture) and then determine which diagnostic study is most appropriate (CT Scan).