Eyes, ears nose and throat: 30 Powerpoint slides
Eyes, ears nose and throat: 30 slides in total
– First PP slide: Topic
– Last PP slide: References, no less than three, within the last five years, and cited using APA style.
– 0 plagiarism
– Body of the presentation:
Includes:
· Summary of the diagnostic studies required or used in the system that is being reviewed (name, indication, teaching to the patient about the procedure and unique considerations)
· Most essential conditions: name, definition, brief pathophysiology, signs and symptoms, diagnostic studies required with positive results that help in the diagnosis of the state, three differential diagnose and management (treatment)
attached powerpoint for example, not to be used
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PowerpointEENT2.pptx
Eye Evaluation
Evaluation of the Eyes
Routine Screening/Comprehensive Eye Exam
Every 1-2 years
>65 years old
without risk factors for eye disease
3-5 years after diagnosis
Patients with DM – type 1
At diagnosis and Annually
Patients with DM – type 2 to assess for diabetic retinopathy
Prior to Pregnancy and at first trimester
women with DM
Clinical Assessment and P.E.
PMHx and FamHx and ocular history
Medications
Systematic approach to examining the eyes and function
Visual acuity
Pupillary response
Intraocular pressure
Ocular alignments and extraocular movements
Visual fields
External structures
Anterior/posterior segments
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Evaluation of the Eyes
S/S of Eye Conditions
Red Eye
Bacterial, viral, allergic fungal infection
Vision Loss and Other Visual Disturbances
Decreased central or peripheral vision, metamorphopsia (distorted images), photopsia (light flashes), or vitreous opacities (floaters)
Ocular Disease
Ocular and Periocular Disease
Any discomfort in or around the eye and may be described as burning, aching, throbbing, boring, stabbing, or irritating
Foreign body sensation
Pain receptors in the eyelids, cornea, conjunctiva, and uveal tract will cause ocular or periocular pain
Any inflammatory disorder of the conjunctiva, superficial layers of the cornea, or uveal tract can cause ocular irritation, burning, discomfort, or frank pain
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Cataracts
An opacification of the lens that distorts the images that are projected onto the retina, resulting in difficulty seeing that may progress to complete loss of sight.
Intervention is indicated when visual acuity has been reduced to a level the client finds unacceptable or when diminished sight adversely affects the client’��s lifestyle.
Assessment findings include:
Blurred vision and diminished color perception (early signs)
Diplopia, reduced visual acuity, absence of the red reflex, and the presence of a cloudy white pupil (late signs)
Age-related: pain and eye redness
Gradual loss of vision
Cataracts
Cataracts
Considerations
The natural lens is surgically removed and (usually) replaced with an artificial lens, one eye at a time.
Administer preoperative eye medications; the client may need to administer the medications at home before the procedure.
After surgery, elevate the head of the client’��s bed 30 to 45 degrees and turn the client on his or her back or to the unaffected side.
Have the client wear an eye patch and orient the client to the environment.
Position the client’s personal belongings on the unaffected side.
Maintain safety.
Provide home care instructions.
GLAUCOMA
What is it?
A disease of progressive optic neuropathy with loss of retinal neurons and their axons (nerve fiber layer) resulting in blindness if left untreated.
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And you thought glaucoma was a disease in which there was too much pressure in the eye! So did most ophthalmologists until several years ago.
GLAUCOMA
How do we diagnose it?
IOP is not helpful diagnostically until it reaches
approximately 40 mm Hg at which level the
likelihood of damage is significant.
Visual fields are also not helpful in the early stages
of diagnosis because a considerable number of neurons must be lost before VF changes can be
detected.
Optic nerve damage in the early stages is difficult
or impossible to recognize.
50% of people with glaucoma do not know it!
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The three mainstays of glaucoma diagnosis are inadequate. The actual intra-ocular pressure is too imprecise, and the changes in the visual field and the optic nerve occur too late to prevent most of the damage.
GLAUCOMA
Cup-to-disk ratio
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No two disks are alike. Signs suggesting glaucoma as seen in the right photo include a large cup, nasalization of vessels, and pallor of the cup. Note the peripapilary depigmentation on the right which can make the true cup:disk ratio difficult to estimate.
GLAUCOMA
Normal
DISK CUPPING
Glaucoma
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In glaucoma of all types, if not controlled. There is progressive enlargement of the cup, increased pallor of the base of the cup, and nasalization of the disk vessels.
GLAUCOMA
TREATMENT GOALS: Reduce pressure to less than or equal to 24 mm Hg with a minimum pressure reduction of 20% from the baseline.
OUTCOME MEASURES: Development of reproducible visual field abnormality or development of optic disc deterioration.
MEDICATIONS USED: beta-adrenergic antagonists,
prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.
OHTS parameters
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Narrow Angle Glaucoma
Onset: 50+ years of age
Symptoms
Severe eye/headache
pain
Blurred vision
Red eye
Nausea and vomiting
Halos around lights
Intermittent eye ache
at night
Signs
Red, teary eye
Corneal edema
Closed angle
Shallow AC
Mid-dilated, fixed
pupil
“Glaucomflecken”
Iris atrophy
AC inflammation
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The classical signs and symptoms of narrow angle glaucoma.
Narrow Angle Glaucoma
Mid-dilated, fixed pupil
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Mid-dilated, fixed pupils and cloudy corneas during an angle closure attack.
Open Angle Glaucoma Aka: chronic simple glaucoma (CSG) and primary open angle glaucoma (POAG)
Risk Factors
IOP Diabetes
Age Myopia
Race Gender
Family history Cardiovascular
Central corneal disease
thickness Hormones
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Open Angle Glaucoma
Onset: 50+ years of age
Symptoms
Usually none
May have loss of central
and peripheral vision
late
Signs
Elevated IOP
Visual field loss
Glaucomatous disk changes
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Remember: most patients with open angle glaucoma have no symptoms. This is the best reason to have periodic eye examinations with pressure checks and optic nerve evaluations.
Normal Tension Glaucoma (NPG, LTG, LPB, NTG)
Similar to OAG but IOP always < 21 mmHg
Higher prevalence of vasospastic disorders,
blood dyscrasias, autoimmune diseases
May be related to episodic hypotension,
hypothyroidism
A diagnosis of exclusion!!!
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Open Angle Glaucoma
HISTORY:
Positive family history
African American and Hispanic background
History of trauma
History of steroid use
Risk factors
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GLAUCOMA
Treatment
Medical
Surgical
Miotics
Beta-blockers
Carbonic anhydrase
inhibitors
Prostaglandin
analogues
Alpha-2 agonists
Argon laser trabeculoplasty
Trabeculectomy
Filtering procedure
Cyclocryotherapy
Cyclolaser ablation
Iridotomy
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No treatment works all the time!
Glaucoma
Considerations
Chronic Glaucoma
Medications that will decrease intraocular pressure will be prescribed. Explain to the client the possible need for lifelong medication use.
Instruct the client to avoid anticholinergic medications (prescribed for gastrointestinal conditions such as gastritis or ulcerative colitis; respiratory conditions such as asthma or chronic obstructive pulmonary disease; genitourinary conditions such as prostatitis or urethritis; and Parkinson disease) and to obtain permission from the physician before taking any over-the-counter medication.
Instruct the client to report eye pain, halos around lights, and changes in vision.
Tell the client that when maximal medical therapy has failed to halt progression of visual field loss and optic nerve damage, surgery will be recommended.
There are five main groups of glaucoma drugs, each acting in a different way to reduce IOP:
A) prostaglandin analogues (bimatoprost, latanoprost, and travoprost) increase uveoscleral outflow
B) beta-blockers consist of two main groups: selective (betaxolol) and non-selective (timolol, levobunolol), both of which decrease aqueous production
C) alpha-2 adrenergic agonists (apraclonidine, brimonidine) decrease aqueous production and increase uveoscleral outflow
d) carbonic anhydrase inhibitors decrease aqueous formation and can be applied topically (brinzolamide, dorzolamide), or systemically (acetazolamide, methazolamide)
E) parasympathomimetics (pilocarpine, carbachol) increases aqueous outflow through the trabecular meshwork by means of ciliary muscle contraction, and may open the drainage angle in angle-closure glaucoma by stimulating the iris sphincter muscle.
Conjunctivitis
Conjunctivitis
Inflammation of the conjunctiva, the transparent mucosal tissue that lines the eye and inner surface of the eyelids
Infectious: viruses and bacteria
Noninfectious: allergy, atopy, or exposure to toxins
Clinical Presentation
Viral: Recent URI or exposure to sick contacts (Adenoviral conjunctivitis)
Ocular S/S: acute onset of a red eye with excessive watery discharge, lymphadenopathy (screen for MRSA, HSV)
Bacterial: thick, purulent discharge, eyes are sticky/glued shut. These symptoms persist throughout the day but are worse in the morning
Allergic: headache, fatigue, possible fam Hx of atopy allergy, bilateral involvement, itching of eyes
Vernal and atopic: more severe s/s of severe itching, burning, and tearing, begins in childhood – resolves in the third decade, blepharospasm and photophobia. Discharge is often white, thick, and ropy
Medication toxicity: contact dermatitis of the lower lids with thickening and scaling of the skin is sometimes seen
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Etiology:
Chlamydia trachomatis and Neisseria gonorrhea- MOST COMMON IN NEWBORNS
Virus: adenoviruses – MOST COMMON in ADULTS & CHILDREN
Bacterial: S. Aureus – MOST COMMON IN ADULTS
IRRITATIVE: topical medications, wind, etc
Autoimmune: example: Sjogrens syndrome
Physical Exam
Visual acuity
Pupillary reaction and EOM’s intact
Edema of eyelids and matted eyelashes
Red eye, conjunctival injection
Foreign body sensation
* pt should not report photophobia and examiner should not see pupillary abnormalities in simple conjunctivitis
Conjunctivitis
Diagnostics
Thorough eye exam
Visual acuity testing
Gram-stained smears and cultures are necessary in the immunocompromised (including neonates) as well as in severe or unresponsive cases
PCR (chlamydial conjunctivitis)
Differential Dxs
Must consider other causes of conjunctival injection – may be benign to potentially sight-threatening
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Conjunctivitis
Management
Viral: artificial tears and cool compresses. Advise considered contagious as long as they are still tearing or for at least 1 week
Bacterial: use discretion in topical Abx Rx. Abx if suspect high infectivity rate (high-risk patients should always receive Abx) trimethoprim–polymyxin B or fluoroquinolone drops, 4 times a day for 1 week.
Systemic Abx for: H. influenzae,
gonoccocal or chlamydial infection
Allergic: avoidance of trigger, oral antihistamine preservative-free artificial tears, cool compresses, and removal of contact lenses. For severe cases addition of antihistamine-vasoconstrictor, mast cell stabilizers
Vernal and atopic: Avoid of triggers, mast cell stabilizers initiated 2 weeks before known allergic S/S develop
Medication toxicity: Eliminate toxic source, treat with preservative-free artificial tears. Short course of topical steroids
Ophthalmologic referral based on assessment of sight-threatening risk
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Prevention:
US Preventative Task Force Services Recommendation:
All newborn infants: Provide prophylactic ocular topical medication for the prevention of gonococcal ophthalmia neonatorum within 24 hours after birth
Preventive medications include 0.5% erythromycin ophthalmic ointment, 1.0% solution of silver nitrate, and 1.0% tetracycline ointment. All are considered equally effective; however, the latter two are no longer available in the United States.
Adults and Children: Frequent hand washing and hygiene
Management:
Avoid irritants
No contact lenses/ replace make-up
Allergic: Pantanol
Bacterial (NON Sexually Transmitted Infection): Tobramycin 3%, erythromycin ophthalmic ointment, etc.
Bacterial (Gonococcal): may need to be hospitalized for IV ABX, if no corneal lesions, ceftriaxone 1 g IM x1 and topical ophthalmic ABX
Neonates: base treatment on culture and sensitivity results
Erythromycin ethylsuccinate PO x 14 days
Special Considerations:
If suspect Herpetic: REFERRAL
Pregnancy or lactation: DO not prescribe doxycycline
If no improvement in 24 hours: REFERRAL
If sever pain, changes in visual acuity: REFERRAL
Blepharitis, Hordeolum, and Chalazion
Blepharitis, Hordeolum, and Chalazion
Blepharitis
Inflammation of the eyelids
Infectious or inflammatory
Chalazion
A chronic, sterile, lipogranulomatous inflammatory lesion of the meibomian gland
Hordeolum
An acute infection of one of the glands in the eyelid
The most commonly associated organism is S. aureus
Clinical Presentation
Blepharitis Sxs: due to ocular tear film instability and dry eye
Sxs: burning, foreign body sensation, tearing, photophobia, itching, redness, discharge, and swollen erythematous eyelids, often worse in the morning
Chalazion Sxs: usually non-painful,
Hordeolum Sxs: usually painful,
In both chalazion and hordeolum there may be cosmetic disfigurement and mechanical ptosis
If large, the lesion may mechanically press on the corneal surface to induce astigmatism and blurred vision
Copyright © 2017 by Elsevier Inc. All rights reserved.
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Blepharitis, Hordeolum, and Chalazion
P.E.
Inspect face, ocular adnexa, and eye (conjunctiva, sclera, palbera)
Inspect eye and lashes for discharge – suspicious for bacterial infection
Palpate eyelids for mass, pain assessment
Diagnostics
Based on clinical findings
Differential Dxs
Sebaceous carcinoma, basal cell carcinoma, squamous cell carcinoma (rare)
Eye syndrome
Conjunctivitis (viral, bacterial, or allergic)
Contact dermatitis
Atopic keratoconjunctivitis
Herpes simplex infection
Preseptal cellulitis
Acute dacryocystitis
Ocular rosacea
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Blepharitis, Hordeolum, and Chalazion Management
Blepharitis:
Warm compresses
Hygiene
Lid scrub kits
Warm water, diluted baby shampoo on cotton tip applicator
Erythromycin or bacitracin ointment
Artificial tears may also be beneficial
Hordeolum:
Self-limited
Frequent application of warm, moist compresses with light massage over lesion.
Daily lid hygiene with lid scrubs is also beneficial
Chalazium:
Self-limited
Chronic chalazium
may require steroid injection
OR surgically removed by ophthalmologist
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Corneal Abrasion
Defect of the epithelial layer of the cornea caused by a mechanical trauma to the surface of the eye
Etiology: Fingernails, paws, paper, branches
Foreign Body: rust, wood, plastic
Contact lens: Improperly fitting, dirty, over-worn, dry eyes with contact lens
RETINAL DETACHMENT
Marina Capak
Mentor: A. Žmegač Horvat
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pulled away from the underlying choroid
small areas of the retina torn =>
retinal tears or retinal breaks
retinal cells deprived of oxygen
if not promptly treated => permanent vision loss
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SYMPTOMS
floaters – bits of debris in field of vision that look like spots, hairs or strings
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SYMPTOMS
floaters
light flashes
shadow or curtain over a portion of visual field
blur in vision
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Can occur as a result of:
trauma
advanced diabetes
an inflammatory disorder, such as sarcoidosis
shrinkage of the jelly-like vitreous that fills the inside of the eye
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vitreous liquid leaks through retinal tear and accumulates underneath retina
retina can peel away from underlying layer of blood vessels
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Factors that may increase risk of retinal detachment:
aging – more common in people older than 40
previous retinal detachment in one eye
family history of retinal detachment
extreme nearsightedness
previous eye surgery
previous severe eye injury or trauma
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TREATMENTS
Retinal tears:
laser surgery (photocoagulation)
freezing (cryopexy)
Retinal detachment:
pneumatic retinopexy
scleral buckling
vitrectomy
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Presentation:
Excruciating pain, inability to open eye, photophobia, tearing, foreign body sensation
Usually unilateral
History of contact lens use, dry eyes
PE:
Increased lacrimation on affected side
Altered integrity of smooth cornea seen as irregular light reflex.
May be visible with the naked eye or with the use of fluorescein staining.
Diagnostic Test:
Fluorescein staining will show epithelial disruption on the cornea
Slit-lamp exam may be required by specialist to determine corneal penetration
Treatment:
Irrigation of normal saline to flush any foreign particles
Patching of eye no longer recommended
Avoid contact lens use until pain free and eye is healed
Topical ophthalmic ABX
Topical NSAIDS (use with caution)
Never use topical steroids- may delay healing
Tetanus Booster if indicated
Impaired Hearing
Impaired hearing is a defect in the detection and/or processing of sound waves
Affects both communication ability and personal safety and can be a socially isolating experience
Hearing loss occurs at all ages
Increases with advancing age
Requires different considerations in children than in adults
Clinical Presentation
Immediate specialist referral to an otolaryngologist or neurologist is indicated for patients with sudden hearing loss
May present as sudden, progressive, or fluctuating in nature
Assess whether unilateral or bilateral
Associated Sxs: otalgia, ear fullness, vertigo, tinnitus, or cranial neuropathies should be documented
Pts’s Med/Fam Hx and medication use should incorporate current and past treatments with oral and IV meds, OTC
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Impaired Hearing
P.E.
Perform a complete HEENT exam
Diagnostics (as indicated)
Rinne and Weber test
Screening audiogram
Tympanometric screening
MRI/CT scan
Differential Dxs
Sudden Causes
Idiopathic sensorineural hearing loss, infections, perilymphatic fistula, ischemia of the inner ear or retrocochlear structures, multiple sclerosis, autoimmune diseases, trauma, chronic renal failure, and sickle cell anemia
Chronic Causes
Presbycusis, noise exposure, familial factors, retrocochlear neoplasm, chronic otitis media, cholesteatoma, otosclerosis, hypothyroidism, diabetes, and chronic renal failure. Differential diagnosis for fluctuating hearing loss includes otitis media perilymphatic fistula, Meniere’s disease, multiple sclerosis, migraine headache, syphilis, autoimmune disorders, and sarcoidosis
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Impaired Hearing
Management (as indicated)
Remove cerumen impaction – spontaneous improvement in hearing
Treat underlying infection, other etiologies
Otolaryngology referral is indicated for patients with hearing deficit associated with trauma, congenital hearing loss, tumors, obstructions of the external auditory canal, nonhealing TM rupture, and otosclerosis. Treatment for otosclerosis may be stapedectomy or sound amplification
TM perforation may heal spontaneously or require a surgical patch or graft
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Earache: Differential Diagnosis
Otitis Externa: Inflammation of the lining of the external ear canal
Bacterial: Pseudomonas aeruginosa, Staph. Aureus, Group A Stre p. pyogenes Fungal agents: Candida, others Symptoms: Pain at external canal, acute, severe at times, pruritus; frequent swimming Physical Findi
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