CAM I Ophthalmology 2 PDF

CAM I: Ophthalmology 2 Professor Boucher South College Where Dreams Find Direction  Learning Objectives  Recognize and explain the basic types and treatment of eye trauma (LO 2, 7).  Describe the etiology, signs, sy...

CAM I: Ophthalmology 2 Professor Boucher South College Where Dreams Find Direction  Learning Objectives  Recognize and explain the basic types and treatment of eye trauma (LO 2, 7).  Describe the etiology, signs, symptoms, and physical examination findings for diabetic retinopathy and hypertensive retinopathy (LO 1-5, 7, 12).  Recognize and describe common ocular abnormalities, including nystagmus and retinal detachment (LO 2, 7).  Describe the visual pathway (LO 1).  Recognize and describe the common abnormalities of the optic nerve and orbital cavity (LO 2, 7).  Describe the signs, symptoms, diagnosis, and treatment of glaucoma (LO 1-5, 7, 12).  Compare and contrast different diseases that may cause blindness (LO 1-5, 7, 12).  Describe the pathophysiology, diagnosis, signs, symptoms, and treatment of cataracts (LO 1-5, 7, 12).  Describe the pathophysiology, diagnosis, signs, symptoms, and treatment of macular degeneration (LO 1-5, 7, 12). Eye Trauma  Open Globe/Ruptured Globe  Ruptured globe (“open globe”)  Blunt or penetrating trauma to the eye, usually from a sharp object or projectile.  Full thickness break of the eye wall = sclera and cornea.  Requires emergent Ophthalmic consultation LEAVE THE EYE ALONE  Can apply eye shield for protection  Do not put anything in the eye  Avoid any pressure on the globe or eye exam procedures  Avoid topical meds  CT scan of orbits  IV antibiotics per ophthalmology  Typically Vancomycin + Ceftazidime Open Globe/Ruptured Globe Orbital Fractures More common in young males; generally caused by assaults, MVCs, or being struck by a ball in the face/eye.  Blowout Fracture  Orbital “Blowout” fracture  History of small, round, high-speed object (ex: baseball) strikes the eye/orbit.  In one study, half of all orbital fractures involved the inferior wall or floor of the orbit.  Symptoms: bruising and soft tissue swelling, pain  Diagnose with CT imaging  Requires ophthalmology referral + hospitalization  Significant consequence of fractures of the orbital floor is entrapment of the inferior rectus muscle and/or orbital fat.  Ischemia and subsequent loss of muscle function may occur either because of entrapment of muscle within the fracture fragment (more likely in children) or as the result of edema and hemorrhage of muscle that have prolapsed through the fracture into the maxillary sinus (more likely in adults) Blowout Fracture Blowout Fracture  Chemical Ocular Injury  Chemical ocular injury  Eye contact with acids or alkalis requires emergency evaluation and treatment to prevent permanent vision loss. Burn severity depends upon the agent involved, duration of exposure, and depth of penetration.  Alkaline substances usually cause more severe damage than acids (can eat through the eye in minutes).  Assume alkali if unknown  Referral to ophthalmology prior to patient leaving office – true ocular emergency  Presents with decreased vision, moderate-to-severe pain, conjunctival redness, inability to open eyelids, and photophobia  Profuse continuous irrigation with water or saline (until neutral pH is achieved, takes approx. 30-60 mins for most injuries)  Morgan lens is commonly used in emergency dept. Chemical Ocular Injury  Retinopathy  What is retinopathy?  A complication of HTN or DM that affects the eyes  Damage to the blood vessels at the light-sensitive tissue at the back of the eye (retina)  Involves abnormal growth of blood vessels in the retina  Leading cause of preventable blindness  Most common cause of vision loss ages 20-74 in many countries  Importance of regular eye exams, especially for those with risk factors.  Symptoms:  Blurred vision  Floaters  Dark or empty areas of vision  Fluctuating vision Retinopathy Hypertensive retinopathy  Diabetic Retinopathy  A microvascular complication of diabetes mellitus (DM)  Damage to retinal blood vessels leads to retinal ischemia and edema  Presentation: asymptomatic until late stages – visual impairment that may progress to blindness  Nonproliferative (early)  Proliferative (late)  Microaneurysms (red dots), leaking capillaries that can then become occluded  Retinal findings:  Dot and blot hemorrhages  Hard exudates  Cotton-wool spots  Diabetic macular edema (DME) Diabetic Retinopathy Diabetic Retinopathy  Diabetic Retinopathy Nonproliferative – early stages – the walls of the blood vessels weaken, and blood can leak into the retina Proliferative – late stages, needs urgent treatment – abnormal new vessels grow onto the retina Diabetic Retinopathy Normal optic disc Diabetic retinopathy changes Diabetic Retinopathy  Diabetic Retinopathy  Screening:  Treatment:  Type 1 DM: initial screening @ 5 years  Optimize blood glucose control after diagnosis  Intraocular anti-vascular endothelial  Type 2 DM: initial screening @ time of growth factor (anti-VEGF) diagnosis, then yearly or PRN  Injections (Ranibizumab,  Risk factors: bevacizumab)  Diabetes obviously  Peripheral photocoagulation (laser)  Poor glycemic control  Surgery  HTN  CKD with proteinuria or anemia  Hypertensive Retinopathy  Retinopathy related to arteriolar sclerosis and chronic elevated blood pressure leading to ischemia  Presentation: asymptomatic until late stages when vision is impaired  Retinal findings:  Copper/silver wiring  Exudates – stellate configuration referred to as “macular star”  Flame-shaped hemorrhages  Subretinal edema, optic disc swelling  AV nicking  Cotton wool spots Hypertensive Retinopathy  Hypertensive Retinopathy Stages: Mild: arteriolar narrowing, AV nicking, copper wiring Moderate: retinal hemorrhages (blot, dot, flame-shaped hemorrhages), cotton wool spots, exudates Severe: moderate retinopathy findings plus swelling of the optic disc (papilledema) Often involves acute changes in increased blood pressure Treatment: Control blood pressure and lipids Laser treatment  The Visual Pathway  To achieve clear vision, light must follow an unhindered path from the front to the back of the eye, traveling through the cornea, aqueous humor, lens, and vitreous humor to the retina.  Refracted by the cornea and lens (and perhaps also by glasses or contact lenses), light is focused onto the retina where it is transformed into an electrochemical signal by photoreceptors and supporting cells.  The signal is transmitted via the optic nerve through the visual pathways to the occipital lobes. The Visual Pathway Visual Field Defects  Optic Neuritis  Optic Neuritis: acute inflammation and demyelination of the optic nerve which results in acute monocular vision loss and pain with eye movement (stretching the optic nerve at posterior aspect of eye)  Monocular vision loss: only one eye is affected - caused by an ocular issue anterior to the optic chiasm (one eye or optic nerve)  Symptoms: acute onset of monocular vision loss/blurred vision and pain in affected eye  Most common cause is Multiple Sclerosis (MS) Optic Neuritis  Optic Neuritis  Exam: documented newly impaired vision, fundoscopy (blurred optic disc)  Presents with a relative afferent pupillary defect (RAPD, also called Marcus Gunn Pupil)  Condition in which pupils respond differently to light stimuli shone in one eye at a time due to unilateral disease of the retina or optic nerve.  Swinging flashlight test link  Pupil dilates instead of constricts when light is swung to the eye  MRI to confirm demyelination of optic nerve  Treatment:  IV methylprednisolone, referral to Neurology Optic Neuritis  Papilledema  Papilledema: swelling of the optic disc secondary to increased intracranial pressure  Classically bilateral  Symptoms: no early symptoms, generally asymptomatic (vision often minimally impaired)  May have symptoms of increased intracranial pressure (headache, dizziness, N/V)  Testing: fundoscopy followed by MRI and perhaps lumbar puncture  MRI to determine underlying cause  Tumor  Brain bleed  Cerebral edema (infection, trauma, bleed)  Obstruction of CSF flow (hydrocephalus)  Idiopathic (pseudotumor cerebri, elevated intracranial pressure without mass lesion)  Treatment: identify and treat the underlying cause to decrease intracranial pressure Papilledema Papilledema Papilledema  Blindness  Common causes of blindness:  Cataracts  Uncorrected refractive errors  PresbyopiaRefractive errors that could be corrected with glasses but have not been  Myopia  Hyperopia  Astigmatism  Glaucoma  Age-related macular degeneration  Diabetic retinopathy  Chronic Vision Loss  Chronic vision impairment in the elderly  Major causes:  Glaucoma  Cataracts  Age-related macular degeneration  Want to be comfortable recognizing risk factors and typical presentation for each process Glaucoma  Front part of the eye is filled with a clear fluid called aqueous humor, made by the ciliary body (made of sugars, vitamins, proteins, nutrients).  The fluid nourishes the cornea and lens, as well as giving the eye its shape.  Glaucoma is caused by an abnormality in the drainage system of this fluid, causing fluid to build up and leading to increased intraocular pressure in the eye.  Glaucoma Acute angle-closure glaucoma  Sight-threatening medical emergency due to increased intraocular pressure (IOP) which is the fluid pressure in the eye  Risk factors: age, family hx, black race, increased IOP  Symptoms: acute, unilateral, onset of severe ocular pain, impaired vision (colored halos or rainbows around light), red teary eye, headache, N/V  Exam – classic triad of symptoms:  Red eye  Hazy cornea  Fixed, dilated pupil  Glaucoma Chronic open-angle glaucoma Impaired outflow of aqueous humor through diseased trabecular meshwork resulting in a gradual increase in IOP with insidious progressive optic nerve damage leading to peripheral visual field loss Common ~ 90% of glaucoma cases Presentation: Risk factors (same as acute angle-closure) Asymptomatic Diagnosed during routine IOP screening and fundoscopic exam demonstrating optic nerve damage Progressive peripheral vision loss central vision loss = glaucoma Progressive central peripheral vision loss = macular degeneration Glaucoma Glaucoma  Glaucoma  Measure IOP using a Tonopen  Commonly performed in ER when indicated  Screening annually begins ~ 40 years old  Normal IOP ~10-21 mmHg  For screening purposes of chronic open-angle glaucoma, measurement of IOP is not valuable and the best indicator relies on elevated cup : disc ratio seen in fundoscopy  Fundoscopic exam: cupping of the optic nerve  Optic cup: disc ratio > 0.5 is suggestive  Glaucoma Acute angle-closure glaucoma Chronic open-angle glaucoma  Treatment: Irreversible disease – management focuses  Must be treated within hours to avoid on slowing progression and preserving irreversible damage to optic nerve quality of life  Focus on decreasing IOP via decreased Treatment: aqueous humor production Focus on reducing IOP and maintaining  Pressure-lowering topical and systemic normal ocular pressure agents are administered Prostaglandin analogs (Latanoprost) –  Topical B-blocker (Timolol) – increase AH outflow decreases IOP via decreased AH Topical B-blocker (Timolol) decrease production without affecting visual acuity production of AH  Miotics/cholinergic (pilocarpine) – Smoking marijuana (cannabis) can affect vision lower IOP – however not clinically indicated because it does not change  Definitive treatment is laser the course of the disease, is short- peripheral iridotomy (performed same acting, and has other adverse effects day by ophthalmologist) – holes in iris  Glaucoma  Glaucoma Medications  Beta blockers – lowers IOP by decreasing production of fluid in the eye (reduces formation of aqueous  Cholinergic agents – lowers intraocular humor by the ciliary body) pressure by increasing aqueous outflow  Timolol, Betaxolol, Careolol (drainage) through the trabecular network  Alpha agonists – work to both decrease  Pilocarpine production of fluid AND increase drainage  Prostaglandin analogs – lowers  Alphagan P (brimodine) intraocular pressure by increasing outflow of fluid from the eye (drainage)  Iopidine  Xalatan (latanoprost) – now  Carbonic anhydrase inhibitors (CAIS) – available in generic reduces eye pressure by decreasing the  Lumigan (bimatoprost), Travatan production of intraocular fluid (aqueous (travaprost), Zioptan (tafluprost) humor)  Acetazolamide Glaucoma  Cataracts  Symptoms: opacity of the lens, causes blurring or distorted vision.  Leading cause of blindness worldwide.  Painless; progression is highly variable  Risk factors: age (usually > 70 yrs. old), smoking, ETOH, UV exposure, diabetes, metabolic syndrome, prolonged drug use (glucocorticoids, statins), HIV/AIDS, and radiation.  Presents with slowly progressive visual impairment  Exam: diminished red reflex, may note clouding of lens, difficulty seeing retina and posterior structures  Treatment:  Generally, very successful treatment with surgical removal.  Initial treatment can include activity modification and observation  Cataracts  Cataracts causes an opacity/clouding of the lens  Visual changes:  Cloudy/blurry  Can’t see well at night  Double vision  Halos around lights  Lamps, headlights seem too bright  Crystalline lens, which is enclosed in a capsule, focuses a clear image on the retina  Grows throughout life – increased cortical fibers increases thickness  Age-related: most persons over the age of 70 will have some degree of cataracts  One of the most successfully treated conditions in all of surgery  Want to ensure that underlying conditions (glaucoma, retinopathy, or macular disease) are not the cause  Macular Degeneration  Age-related Macular degeneration (AMD)  Leading cause of visual impairment and vision loss in developed countries  Symptoms: gradual vision loss, blurry vision, mostly affecting central vision, so that things in the center look blurry.  Dry AMD – more common (85-90%), more chronic, lose vision slowly  Wet AMD – less common (10-15%), more acute, vision loss can happen quickly  Risk factors: aging (>65 yrs. old), smoking is the strongest modifiable risk factor for developing AMD  Treatment: special combination of vitamins and minerals (AREDS formula), smoking cessation (slows progression)  Patients with wet AMD can be treated with anti-VEGF drugs which have developed significantly in past two decades  Macular Degeneration  Age-related  Painless loss of central vision  Decreased as wavy or distorted vision  Difficulty driving and reading  Central -> peripheral vision loss  Fundoscopy: areas of retinal depigmentation and presence of yellow retinal deposits (drusen)  Screening: Amsler Grid test result  Most common cause of central visual loss and permanent blindness in the elderly Macular Degeneration *Defining feature of macular degeneration* Macular Degeneration Macular Degeneration  Giant Cell Arteritis  Giant Cell Arteritis, also known as Temporal Arteritis, is an inflammation of the lining of the arteries near your temples.  Risk factors: age (> 60-70 years old) and strong correlation with Polymyalgia Rheumatica (PMR)  Never occurs in individuals under 50 years of age  Symptoms: new onset headaches, scalp tenderness, claudication (jaw pain), unexplained fever, and vision problems  Transient or permanent monocular vision loss  Left untreated, can cause blindness  Diagnostic studies: elevated ESR (sed rate) and CRP levels  Treatment: IV steroids (methylprednisolone), hospital admission for temporal artery biopsy Giant Cell Arteritis  Retinal Detachment  Retinal detachment – medical emergency in which thin layer of tissue at the back of the eye pulls away from its normal position. Separates retinal cells from the blood vessels that provide oxygen and nourishment to the eye.  Hallmark presentation:  Flashes of light (photopsia)  Floaters  Sudden appearance of many floaters  Painless, sudden vision loss  A curtain-like shadow descending over the visual field  Mostly spontaneous  Often presents with a peripheral field defect  Risk factors: myopia (nearsightedness), aging (> 50 years old), family history, previous eye surgeries Retinal Detachment  Retinal Detachment  The longer is goes untreated, the greater the risk of permanent vision loss in the affected eye.  Testing:  Fundoscopy  Ultrasound  Treatment:  Ophthalmologic emergency  Surgery: pneumatic retinopexy (cryoretinopexy followed by an injection of air bubble)  Keep patient supine, head turned toward side of detached retina. Retinal Detachment Retinal Detachment  Retinoblastoma  Retinoblastoma  Rare malignant eye cancer that forms in the back of the eye (retina)  Most commonly found in children  Anyone with family history should be screened  Physical exam: absent red reflex or if pupil appears white (when light is shined upon it) Retinoblastoma Visual Field Defects Visual Field Defects Visual Field Defects Visual Field Defects Visual Field Defects  9 Steps For Evaluation The Red Eye 1. Visual acuity: normal or not? 5. Fluorescein stain cornea for disruption 2. Visual inspection – pattern of redness 6. Anterior chamber Subconjunctival hemorrhage, conjunctival Estimate depth as normal or shallow hyperemia, ciliary flush, etc. Detect layered blood (hyphema) or pus 3. Presence of conjunctival discharge (hypopyon) Profuse or scant? Purulent, mucopurulent, serous? 7. Assess pupils for size, symmetry, 4. Detect corneal opacities with pen light, response to light transilluminator, or slit lamp 8. If elevated IOP suspected and reliable Corneal ulcer tonometer available, measure IOP Corneal abrasion Omit if obvious external infection Irregular corneal reflection 9. Detect the presence of proptosis, eyelid malfunction, or any EOM limitations Differential Diagnosis For The Eye Let’s Practice Some PANCE Questions! Let’s Practice Some PANCE Questions! Let’s Practice Some PANCE Questions! Let’s Practice Some PANCE Questions!