Disorders of Vision-Module 8 Part 2

Conjunctivitis

• Inflammation of the conjunctiva—Common eye disorder

• Viral or bacterial, allergy or irritant (physical or chemical) can produce inflammation (commonly called “pink eye”)

• Due to direct contamination (touch, towels, eye drops)

• Severity—Mild to severe (redness to purulent)

Conjunctivitis Symptoms and Diagnosis

• Scratching or burning sensations, itching, photophobia

• Pain mild as compared to corneal abrasions or glaucoma

• Discharge may be present—Mucopurulent with bacteria or fungus

• Diagnosis: H&P, Ophthalmologic exam, Cultures

Allergic

• Seasonal (hay fever)

• Manifestations—Itching, tearing, redness

• Treatment—Avoid allergen, cold compresses, eye washes

• Topical medications—Mast cell stabilizers, histamine antagonists, nonsteroidal anti-inflammatories

• Oral medications—Second generation antihistamines

Bacterial

• Yellow–green drainage, eyelids sticky, lids irritated

• Treatment—Local antimicrobials

• Self limiting—1–3 days with antimicrobials; 10–14 days without treatment

• Hyperacute infections—Severe, sight threatening infections

Gonorrheal conjunctivitis

• Redness, edema, lid swelling, swollen preauricular lymph nodes

• Treatment is systemic and local antimicrobials based on culture/sensitivity

Chlamydial infection in newborns from infected mothers

• Trachoma (chlamydia)—More severe causing corneal ulceration and scarring

• In developing countries—Due to direct contact, fomites, flies

• Leading cause of preventable blindness in the world

Viral

• Highly contagious—Adenovirus most common

• Children more than adults

• Clinical manifestations: Hyperemia, tearing, minimal exudate, Associated with upper respiratory tract infections

• Also due to direct contact, personal items, swimming pools

• No treatment—Lasts 2 weeks (cool compresses and artificial tears). No use of contact lenses until infection resolved

• Prevention—Hygiene measures, no sharing personal items (makeup)

Corneal Trauma

• Epithelial layer damage is less serious (can regenerate)

• Mild epithelial abrasions are very painful, but will heal without scarring

• Endothelial layer damage more serious: Edema can cause loss of transparency and loss of visual acuity. Infection may occur

• Injury to basement membrane can cause scar formation and reduction of light transmission

Keratitis

• Inflammation of the cornea

• Causes—Due to infection, contact lens misuse, defects in tearing

• Clinical manifestations: Pain, photophobia, hyperemia. May cause corneal ulceration

• Categories: Infectious—Bacteria, virus, fungi. Noninfectious—Eye trauma, chemical exposure, ultraviolet exposure

Herpes Simplex Keratitis

• Leading cause of corneal scarring and blindness in the world

• HSV-1 type are most common (HSV-2 in neonates born to infected mother)

• May be a primary or recurrent infection

• Clinical manifestations: Irritation, photophobia, tearing initially, Visual reduction results. May have history of fever blisters

• Treatment: Can be corrected without scarring if caught early (epithelial layer affected). Topical antiviral agents

Varicella Zoster Ophthalmicus

• Herpes zoster—Can affect the ophthalmic division of the trigeminal nerve

• 10–25% of all herpes zoster cases

• More common in immunocompromised

Varicella Zoster Ophthalmicus Treatment and Symptoms

• Herpes zoster—Can affect the ophthalmic division of the trigeminal nerve

• 10–25% of all herpes zoster cases

• More common in immunocompromised

• Clinical manifestations: Fever, headache, burning and itching in the periorbital area. Skin eruption in 1–2 days. Rash is vesicular, then pustular, then crusting

• Treatment—High dose of oral antivirals

• Prevention with herpes zoster vaccine

Intraocular Pressure and Glaucoma

• Glaucoma—An optic neuropathy that is the leading cause of blindness worldwide

• Normally—Rate of aqueous humor secretion equals the outflow

• Causes—Congenital or acquired mechanical obstruction of aqueous humor outflow

• Two types: Primary open-angle glaucoma. Primary angle-closure glaucoma (rarer)

• Pressure range is 10–21 mmHg

• Clinical manifestations—Visual field loss

Open-Angle Glaucoma Pathology and Risk Factors

• Increased intraocular pressure measurements or optic disc abnormalities

• Damage to the optic nurse cup precedes visual loss (therefore, annual exams are important)

• Iridocorneal angle remains open

• Trabecular meshwork abnormality decreases the rate of aqueous humor reabsorption

• Gradual buildup of aqueous humor and pressure

• Asymptomatic and chronic

• Progressive optic nerve damage and vision loss

• Risk factors—Age of 40 or older, Black race, family history, myopia

Open angle Glaucoma Diagnosis and Treatment

• Diagnosis—Applanation tonometry (pressure measures), eye exams

• Treatment—Medication (eye drops) or surgically increase the outflow channel

Angle-Closure Glaucoma Pathophysiology and Risk Factors

• Iridocorneal angle is closed so aqueous humor cannot flow in to the trabecular meshwork

• Iris is displaced forward

• Usually due to iris thickening caused by pupil dilation

• Rapid buildup of aqueous humor in the anterior chamber

• More common in people of Asian or Inuit descent

Angle-Closure Glaucoma manifestations, treatment, and diagnosis

• Sudden increases in intraocular pressure

• Can follow prolonged pupil dilation

• Ocular pain, blurry vision, pupil may become large and fixed—Can resolve spontaneously

• If attacks are repeated or prolonged—Channel damaged or can close

• Eye—Reddened, corneal edema, severe unilateral headache with nausea and vomiting

Angle Closure Glaucoma Diagnosis and Treatment

• Diagnosis: Ophthalmologic exam. This is an emergency

• Treatment: Reduce pressure, laser to create an opening between the anterior and posterior chambers in the involved eye. May be needed on the other eye to prevent glaucoma in the healthy eye

Hyperopia-Disorder of Refraction

• Farsighted

• Anteroposterior dimension of the eye is too short

• Images at a distance are focused, but near images are blurred

• Treatment/Diagnosis: Eye exam, corrective lenses.

Myopia-Disorder of Refraction

• Nearsighted

• Anteroposterior dimension of the eye is too long

• Images at a distance are blurred, but near images are in focus

• Diagnostics and treatment—Ophthalmologic exams and corrective lenses

Presbyopia- Disorder or Accommodation

• Decrease in accommodation due to aging (the lens thickens and becomes less elastic)

• Inability to read fine print

• Diagnostics and treatment—Ophthalmologic exams and corrective lenses

Cataracts

• Lens opacity that decreases transmission of light to the retina. Most are bilateral

• Causes—Aging (>60), heredity, systemic diseases (diabetes), long term sunlight exposure, heavy smoking, corticosteroids

• Diagnosis—Report of visual impairment, physical examination

• Treatment—Bifocals, magnification, increase lighting, ultimately surgery

Childhood Cataracts

• Congenital—Appears at birth, some to diabetic mothers, most not progressive or dense enough to cause impairment

• Acquired (one-third metabolic or infectious, one-third idiopathic)—If severe must be corrected within 2 months to prevent blindness

Retinal Blood Supply—Retinopathies

• Problems in small retinal blood vessels causing

• Microaneurysms: Outpouchings of retinal vasculature. Results in plasma leakage causing edema

• Neovascularization: New vessels form which are more fragile. May lead to hemorrhages

• Opacities: Loss of retinal transparency due to hemorrhage or exudates (from inflammation)

Diabetic Retinopathy Risk Factors

• One of leading causes of blindness in the Western world

• Risks—Hyperglycemia, hypertension, hypercholesterolemia, and smoking

Diabetic Retinopathy Nonproliferative

• onfined to retina

• Leakage of fluid into retina causes edema and decreased visual acuity

Diabetic Retinopathy Proliferative

• Neovascularization causing leakage and pulling on the retina

• Can lead to progressive blindness

• Prevention—Annual examination, blood glucose control, hypertension and hypercholesterolemia control

• Treatment—Laser treatment, vitrectomy

Hypertensive Retinopathy

• Hypertension causes thickening of the arteriole walls and decrease in capillary perfusion pressures

• If severe and uncontrolled, causes microaneurysms, retinal hemorrhage, exudates, and swelling of the optic disc

• Treatment—Control of hypertension

• Advanced hypertensive retinopathy is predictive of death from stroke

Retinal Detachment

• Separation of the neurosensory retina from the pigment epithelium

• Fluid accumulates between the two layers

• An emergency event

Retinal Detachment Exudative

• Due to accumulation of fluid in the subretinal space

• Resolves once underlying cause is successfully treated

Traction Retinal Detachment

• Mechanical force on the retina

Retinal Detachment Rhegmatogenous

• Most common type

• Full thickness break in the retina

• Risk factor of age (63% are in 80s) and myopia

Retinal Detachment Symptoms, Diagnosis, Treatment

• Clinical manifestations—Painless vision changes

• Flashing lights, sparks, floaters (early)

• Progresses to shadow/dark curtain progressing across visual field

• Diagnosis—History and ophthalmologic exam of the retina

• Treatment—Vitreoretinal surgery

Macular Degeneration Risk Factors and Types

• Central portion of the retina is affected, resulting in loss of central vision

• Age related are most common (over 50)

• Risks—Female, white race, smoking, obesity, dietary factors, genetic links possible

• Types: Atrophic nonexudative—Dry. Exudative—Wet

Atrophic Nonexudative

• No leakage of blood or serum

• Degeneration of outer retinal and pigmented epithelium

• Visual impairment variable

• Close follow up (exudative form may develop)

Exudative, diagnosis and treatment

• Choroidal neovascular membrane forms

• Blood vessels leak; new vessel walls weak

• Fluid buildup pushes the retina away from pigmented epithelium

• Scar tissue causes loss of vision

• Diagnosis—Report by patient (changes in central vision, blurring, scotomata)

• Treatment—Laser therapy, intravitreal injections of anti-VEGF meds

Visual Field Defects

• Visual fields

  • The area visible during fixation of vision in one direction

• Defects are due to retinal damage, optic pathway or visual cortex damage

• Anopia—No vision in one eye

• Hemianopia—No vision in half of visual field of one eye

• Quadrantanopia—No vision in one quarter of visual field of one eye

• Homonymous hemianopia—Same half of visual field affected in both eyes

• Heterogenous hemianopia—Different halves of field in both eyes

Eustachian Tube Disorders-Abnormal Patency

• Tube does not close or close completely

• Allows air and secretions into the tube which leads to middle ear infections

Obstruction-Eustachian Tube Disorders

• Mechanical

• Impacted cerumen (earwax)—Accumulates and hardens

• Reversible hearing loss

• No symptoms unless the cerumen irritates the tympanic membrane. Pain and itching may result

• Treatment—Gentle irrigation with warm water or a ceruminolytic agent

Inflammation Otitis Media (OM) Risk and Types

• Inflammation of the middle ear

• Two types: Acute otitis media (AOM)—Rapid onset of middle ear infection. Otitis media with effusion (OME)—Presence of fluid in the middle ear without acute infection

• Risks: Mostly children three months to three years and again around age five. Smoking in the house, premature children, daycare attendance, males, family history, bottle feeding, cleft lip/palate

• Typically follows upper respiratory tract infection

Acute Otitis Media Symptoms

• Rapid onset, ear pain, fever, hearing loss

• Infants—Ear tugging, irritability

• Older children—Rhinorrhea, vomiting, diarrhea

Acute Otitis Medias Diagnosis and Treatment

• Diagnosis: Ear pain, tympanic membrane redness, middle ear effusion, tympanic membrane may perforate

• Treatment: Pain management, Myringotomy to relieve pressure, Observe without antibiotics for 48–72 hours, then antibiotics if worsens

Otitis Media With Effusion Symptoms

• May be asymptomatic, intermittent ear pain, fullness, popping

• Infants—Ear rubbing, irritability

• Hearing loss may interfere with school and language development

Otitis Media With Effusion Treatment and Diagnosis

• Diagnosis: H&P, Presence of middle ear effusions

• Treatment: Resolves in 3 weeks to 3 months, May be only observation or observation with antibiotics, May add corticosteroids

Otitis Media With Effusion Complications

• Hearing loss, mastoiditis, cysts in the middle ear, intracranial complications (rare)

Tinnitus

• Abnormal ear or head noises not produced by external stimulus

• Ringing, hissing, humming, roaring

• Constant, intermittent, unilateral or bilateral

• Typically in older adults or those who work in loud areas

Objective Tinnitus

• Can be heard by observer (vascular)

Subjective Tinnitius

• Not detectable by others

• Due to impacted cerumen, meds (aspirin), caffeine, nicotine, hypertension, atherosclerosis, ear infections/inflammation

• May be noise induced

Treatment of Tinnitus

• Eliminate causative agents (meds), eliminate cheeses, red wine, MSG

• Use of low noise generators

Hearing Loss

• Affects 36 million Americans of all ages

• Classified from mild to profound

• Leads to social isolation and depression, can have safety implications

• Genetic or acquired, sudden of progressive, unilateral or bilateral, partial or complete, reversible or irreversible

Conductive Hearing Loss

• Stimuli not conducted to the inner ear

• Sound is blocked

Sensorineural Hearing Loss

• Stimuli conducted to the inner ear

• Cochlear apparatus or auditory nerve abnormalities prevent conduction to the brain

• Medications that are causative agents—Aspirin, aminoglycosides, antimalarial, chemotherapy, loop diuretics

Hearing loss diagnosis and Treatment

• Diagnostics: H&P. Hearing testing

• Treatment: Hearing aids, Cochlear implants

Vertigo

• Illusion of motion caused by central or peripheral vestibular disorders

• Objective—Person stationary, environment in motion

• Subjective—Person in motion, environment stationary

• Motion sickness—Normal physiologic vertigo. Repeated rhythmic stimulation causing vertigo, nausea, vomiting (riding in a car, plane, boat)

• Benign paroxysmal positional vertigo—Due to change in head position

Ménière’s Disease

• Triad of hearing loss, vertigo, tinnitus

• Other manifestations—Pallor, sweating nausea, vomiting

• Vertigo is violent—Unable to it or walk; individual needs to lie quietly with head in a fixed position

• Hearing loss as disorder progresses

• Diagnosis by audiogram, vestibular testing

• Treatment—Medications to decrease vestibular activity, diuretics, low sodium diet, steroids

Vestibular System

• Located in the inner ear, primarily responsible for balance

• Disorders are characterized by nystagmus, vertigo, tinnitus, nausea and vomiting, and autonomic nervous system manifestations

Vestibular System Conintued.

• Normal with head movement and rotational movements

• Spontaneous nystagmus is pathological

  • Fatigue

  • Stress

  • Central nervous system pathology

Vertigo

• Illusion of motion caused by central or peripheral vestibular disorders

• Objective—Person stationary, environment in motion

• Subjective—Person in motion, environment stationary

• Motion sickness—Normal physiologic vertigo. Repeated rhythmic stimulation causing vertigo, nausea, vomiting (riding in a car, plane, boat)

• Benign paroxysmal positional vertigo—Due to change in head position

Ménière’s Disease

• Triad of hearing loss, vertigo, tinnitus

• Other manifestations—Pallor, sweating nausea, vomiting

• Vertigo is violent—Unable to it or walk; individual needs to lie quietly with head in a fixed position

• Hearing loss as disorder progresses

• Diagnosis by audiogram, vestibular testing

• Treatment—Medications to decrease vestibular activity, diuretics, low sodium diet, steroids