HEENT 1-5 only Flashcards

1
Q

What are some causes of orbital fractures?

A

Motor vehicle accidents, industrial accidents, sports related facial trauma, assaults (domestic violence)

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2
Q

What are the 7 bones of the orbit?

A
  1. Sphenoid
  2. Zygoma
  3. Maxilla
  4. Ethmoid
  5. Palantine
  6. Lacrimal
  7. Frontal
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3
Q

What is another name for the zygoma bone?

A

Lamina papyrcea

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4
Q

What makes up the superior wall of the orbit?

A

Frontal and sphenoid bone (lesser wing)

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5
Q

What makes up the inferior wall of the orbit?

A

Maxilla, zygomatic and palantine bones

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6
Q

What makes up the medial wall of the orbit? (thinnest)

A

Ethmoid, maxilla, lacrimal, sphenoid

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7
Q

What makes up the lateral wall of the orbit? (thickest)

A

Zygomatic and sphenoid bone

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8
Q

Some additional orbital structures include

A

Eye, extraocular muscles, sinuses, medial/lateral canthal ligaments, nerves, fat

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9
Q

Lateral rectus muscle action

A

abduction

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10
Q

Medial rectus muscle action

A

adduction

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11
Q

Superior rectus muscle action

A

upward and inward

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12
Q

Inferior rectus muscle action

A

downward and inward

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13
Q

Superior oblique muscle acion

A

rotate inferior and lateral

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14
Q

Inferior oblique muscle action

A

rotate superior and lateral

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15
Q

What muscle attaches to the eyelids and allows for eyelid raise?

A

Levator palpebrae

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16
Q

The three sinuses involved in the orbit?

A

Maxilla, frontal, ethmoid

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17
Q

What is the medial canthal ligament?

A

Attaches to the corner of the tarsal plate to the orbital wall

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18
Q

What is the lateral canthal ligament?

A

Attaches to the lateral aspect of orbital wall

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19
Q

What can disruption of the two canthal ligaments cause?

A

Malpositioning of the eyelids (entropion/ectropion)

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20
Q

What makes up the lacrimal duct system?

A

Lacrimal gland, sac, and the nasolacrimal duct

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21
Q

The infraorbital nerve innervates what?

A

The lower eyelid, nose and upper lip

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22
Q

The supraorbital nerve innervates what?

A

Upper eyelid, forehead and scalp

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23
Q

What structures are associated with the superior orbital wall? (2)

A

Frontal sinus, supraorbital nerve

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24
Q

What structures are associated with the inferior orbital wall? (4)

A

Inferior oblique muscles, inferior rectus muscle, maxillary sinus, infraorbital nerve

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25
What structures are associated with the lateral wall? (1)
Lateral canthal ligament
26
What structures are associated with the medial wall? (5)
Medial rectus muscle, ethmoid sinus, medial canthal ligament, lacrimal duct system
27
What are the types of orbital fractures?
Orbital zygomatic fracture, Nasoethmoid fracture (NOE), orbital roof fracture (rare), *orbital floor fracture*
28
What is the most common type of orbital fracture?
Orbital floor fracture
29
Blowout fracture
Orbital floor fracture without fracture of the orbital rim with herniation of contents
30
What can happen in a blowout fracture?
Bone defect is filled w/soft tissue and fat from orbit, alters support mechanism for EOM, nerve damage can result
31
Impure blowout fracture
fracture line extends to orbital rim
32
Trapdoor blowout fracture
bone fragments involving the central area of bone
33
Most common type of blowout fracture?
Inferior floor
34
Blow-out fracture complications include what
Entrapment of inferior rectus, damage to infraorbital nerve
35
How can we assess orbital fractures?
History-mechanism of injury, inspecting face and eye, palpating crepitus and for sensation deficit
36
Orbital fracture symptoms
Facial pain, ocular pain on movement, neuropraxia, diplopia, color changes, floaters hazy vision clouds fog, flashers veil or curtain, foreign body sensation
37
What will be inspected for an orbital fracture exam?
Periorbital edema and ecchymosis, a depression/defect of the orbit, epistaxis or CSF leakage
38
What will be palpated during an orbital fracture exam?
Nerve neuropraxia (loss of sensation), emphysema, pain, step-off deformity
39
What test can be done for an orbital fracture involving the visual acuity?
Snellen chart-progressive loss may mean increased IOP or optic nerve injury
40
Physical exam findings for an orbital eye fracture
Lid lacerations, periocular ecchymosis, exophthalmos/proptosis (bulging eye), hypoglobus (blood in ant chamber), traumatic mydriasis, canthal ligament disruptions
41
Other physical exam findings of an orbital eye fracture
Epipora (tearing of eye w/no drainage), corneal abrasion, ruptured globe, vitreous hemorrhage, retinal detachment/tears, EOM entrapment
42
What is the gold standard to diagnose an orbital fracture?
CT scan of the orbit
43
What view is best for an orbital fracture (CT)
Axial view: for frontal fractures, NOE fractures, zygomatic arch, vertical orbital walls Coronal view: orbital roofs, orbital floors, ptyergyoid plates
44
Some other additional diagnostic exams for an orbital fracture
Forced ductions test (specialist needs to preform), fluorescein stain, hertel exophtalmometer
45
Major complications of an orbital fracture associated with blindness
Ruptured globe, hyphema, retinal injury (detachment), optic nerve sheath hematoma, glaucoma
46
Major complications of an orbital fracture associated with EOM entrapment?
Orbital floor: inferior rectus | Lateral wall: medial rectus
47
Major complications of an orbital fracture associated with orbital dystopia/cosmetic issues?
Enopthalmos (eye pushed back), hypoglobus
48
Other complications that can arise from an orbital fracture
Long term diplopia, infection, neuropraxia, intracranial bleed (superior orbit)
49
Treatment options for an orbital fracture
Nonsurgical, surgical (controversial for indications, emergent vs. non emergent)
50
Non surgical initial management for orbital fracture
Ice for 48 hours, elevation of HOB, nasal decongestants (increase drainage), broad antibiotics, AVOID aspirin and nose blowing, +/- steroids for orbital edema w/diplopia. Follow up w/ophthalmologist in 7 days
51
Anterior chamber of the eye
Fluid-filled space of Aqueous humor. bordered by cornea, iris, angle and lens
52
What can interrupted aqeuous flow by blood cause?
Increased IOP -> blindness
53
Hyphema
Grossly visible blood in the anterior chamber. Bleeding from tears on the vessels of the ciliary body or iris
54
How can hyphema occur?
Trauma and spontaneous (pts with underlying conditions)
55
What are some differential diagnoses for hyphema?
Corneal abrasion, retinal detachment, globe rupture, glaucoma
56
Symptoms of hyphema
Decreased visual acuity, photophobia, pain
57
Physical exam findings of hyphema
Layer of blood in ant. chamber, decreased visual acuity, photophobia, anisocoria, elevated intraocular pressure
58
Anisocoria
Mydriasis, uneven pupils
59
What tools are used to diagnose hyphema?
Ophthalmoscope, slit lamp, tonopen* (very difficult to use)
60
Treatment of hyphema
Eye shield, elevate HOB 30 degrees at bed rest, cycloplegia (paralyze the eye), bed rest, pain control PO, control N/V with antiemetics, 5% require surgery
61
What would 5% of pts with hyphema need surgery for?
To evacuate the clot
62
What is used to paralyze the eye for treatment of hyphema?
Cyclopentolate or homatropine
63
Follow-up for hyphema
Referral to Ophthalmologist ALWAYS
64
What is hyphema emergent?
If: open globe, orbital compartment syndrome, large hymphemas (grade 3 or 4), hyphemas associated with bleeding dyscrasia
65
What are some complications of hyphema?
Intractable glaucoma: permanent vision loss and blindness, 2ndary hemorrhage (worse prognosis), posterior or peripheral synechiae, optic atrophy
66
Posterior synechiae
Complication of hyphema, when the iris adheres to the lens
67
Peripheral synechiae
Complication of hyphema, when the iris adheres to the cornea
68
What is the most frequent cause of visits for ophthalmic emergencies?
Corneal foreign body
69
Corneal foreign body symptoms
Pain, foreign body sensation, photophobia, tear, red eye, blurred vision
70
Corneal foreign body physical exam
Visual acuity, inspection of eye and eyelid (evert), slit lamp exam, fluorescein stain uptake (woods lamp or slit lamp)
71
Corneal foreign body physical exam findings
Normal/decreased acuity, conjunctival infection, ciliary injection, VISIBLE FOREIGN BODY, rust ring, epithelial defects w/stain w/fluorescein, anterior chamber cell/flare, excessive tear production, corneal edema
72
What is the Seidel test?
Tests for corneal perforation, can be in an exam finding for a corneal foreign body
73
Differential of corneal foreign body
Keratitis, intraocular foreign body, corneal abrasion
74
Corneal foreign body removal treatment
Apply topical anesthetic first, irrigation (morgans lens or direction irrigation), cotton Qtip, sterile needle tip or automatic burr
75
How do you remove a rust ring?
Experienced clinicians do this using a slit lamp, best to refer to opthalmologist in this case
76
Corneal foreign body medical management
Topical antibiotic; erythromycin or ciprofloxacin, topical cycloplegic, avoid contact lens, eye patch, tetanus
77
What is a corneal abrasion?
Any defect in the corneal surface
78
How many layers does the cornea have?
6, endothelium mostly involved w/abrasions
79
What is the cornea innervated by?
Deeply innervated by sensory fibers of the trigeminal nerve
80
Corneal abrasion symptoms
Pain foreign body sensation, photophobia, tear, red eye, burred vision
81
Corneal abrasion differential diagnosis
Acute globe rupture, retained foreign body, infectious keratitis, corneal ulcer, acute angle glaucoma
82
Corneal abrasion physical exam
Visual acuity, inspect eye and evert the lids, slip lamp eye exam, fluorescein stain (woods lamp, slit lamp)
83
Corneal abrasion physical exam findings
Normal/decreased visual acuity, conjunctival injections, visible foreign body, rust ring, epithelial defects w/stain w/fluorescein, ant. chamber cell/flare, excessive tear production, corneal edema
84
Corneal abrasion treatments-antibiotics
Topical: Mainstay of treatment* | ointment preferred, Erythromycin. For contact lens: Ciprofloxacin drops
85
Corneal abrasion pain control treatment
Mild to mod: NSAIDs PO or topical (diclofenac/ketorolac) Severe: Oral opioids for 48 hours Cycloplegics: Prevents pupillary constriction
86
Corneal abrasion follow-up
No follow-up needed, heal 24-48 hours
87
When would you have a corneal abrasion pt follow-up with an opthalmologist?
Large abrasions, contact lens wearers, rust ring, abrasion in young children, abrasions with vision changes
88
What are the infectious causes of corneal ulcers?
VIRAL, bacterial, fungal, amoebas
89
What are the non-infectious causes of corneal ulcers?
Exposure keratitis: Exophthalmos, Bells palsy with lid lag, allergic disease, severe dry eye, inflammatory/autoimmune, VitA deficiency
90
Bacterial causes for corneal ulcers
Pseudomonas, moraxella liquefaciens, strep, MRSA Contacts: Pseudomonas DM, alcoholics, immunosuppressed: Moraxella
91
Viral causes for corneal ulcers
HSV/Zoster
92
Amoebic causes for corneal ulcers
Acanthamoeba, contaminated water, contact lens with poor hygeine
93
Corneal ulcer risk factors
Contact lens, previous eye surgery, eye injury, Hx of HSV, immunocompromised, topical or systemic steroid use
94
Corneal ulcer symptoms
Pain, photophobia, tearing, reduced vision, lid and ocular swelling, injected conjunctiva, injected eyelid, foreign body sensation, miotic pupil, clear or mucopurulent discharge
95
Corneal ulcer physical exam
Visual acuity, slit lamp, fluorescein stain
96
Corneal ulcer physical exam findings
Punctate or diffuse branching dendritic lesions (HSV/Zoster), Corneal ulceration (varying patterns), Hypopyon (pus in ant. chamber), anterior cell/flare
97
Corneal ulcer diagnosis
Slit lamp and fluorescein stain, culture and gram stain or PCR (done by ophthalmologist)
98
Corneal ulcer treatment
Aggressive! Always place on Abx unless dendritic pattern-acyclovir, PROMT referral to opthalmologist 24 hours
99
Bacterial Abxs used for corneal ulcers
Fluoroquinolone*** Fluconazole for fungal, topical acyclovir for viral
100
Pain management for corneal ulcer
Cycloplegics topical or oral NSAID
101
Corneal ulcer complications
Corneal scarring, corneal perforation, anterior/posterior synechiae, glaucoma, cataracts, blindness
102
What are the two kinds of Otitis media?
1. AOM: acute otitis media | 2. OME: otitis media with effusion (chronic)
103
What is the gold stand for the diagnosis of OM?
Pneumatic otoscopy
104
Acute or new OM is what?
When the symptoms have been going on for LESS THAN or equal to 48 hours
105
Severe OM is what?
Toxic/sick appearing child, persistent otalgia longer than 48 hours, temp higher than 102.2 in past 48 hours
106
MEE
Middle ear effusion: fluid behind tympanic membrane
107
What are the diagnostic features of AOM?
mod-severe bulging of the TM or otorrhea (discharge from ear), mild bulging TM and recent ear pain OR intense redness
108
What are the diagnostic features of OME?
MEE without signs or symptoms of acute ear infection, tympanocentesis and pneumatic otoscopy (fluid sitting behind ear)
109
AOM possible pathogens
Strep pneumoniae and H.influenza most common** M.catarrhalis, viruses and ostiomeatal complex dysfunction
110
OME pathophys
Ostiomeatal complex/eustachian tube dysfunction, sequelae of AOM, viral, bacterial antigens, biofilm
111
OME management
Watchful waiting: for children that are not at increased risk for speech language or learning problems Tubes, surgery, prednisone oral or topical, antihistamines/decongestants
112
What is the surgery like for OME?
Myringotomy with tympanostomy tube insertion, tympanocentesis (stick needle in to drain out fluid), adenoidectomy
113
Out of the OME management, which are not recommended to do, but are still given?
Prednisone oral or topical, and the antihistamines/decongestants
114
Severe AOM
Abx if the child is greater than 6 mos, with mod-severe signs OR symptoms OR a temp higher than 102.2
115
Nonsevere AOM
Abx or observe in 6-23 mos if unilateral if and only if you have good follow up Abx greater than 24 mos if bilateral Abx or observe if greater than 24 mos
116
AOM treatment
1st line: Amoxicillin. Alternate: Quinolone drops 2nd choice: Augmentin, Bactrim, 2nd or 3rd gen ceph Ceftriaxone: if patient has severe vomiting
117
Other AOM treatments
Azithromycin, Clindamycin
118
AOM Management
Pain relief: Acetaminophen, ibuprofen, Auralgan Topical decongestant: not recommended Cold meds: not for under 2yo, probably not under 4yo, older then 4 maybe
119
AOM Follow-up
Improvement expected in 24-48 hours, Re-evaluate in 2 weeks
120
AOM prophylaxis
Penumococcal vaccine, breast feeding, smoke-free environment, no bottles in bed Abx prophylaxis: Amox or Sulfasoxazole (not recommended)
121
How does a TM perforation occur?
Blows to the ear, severe atmospheric overpressure, exposure to excessive water pressure, improper attempts at wax removal or ear cleaning
122
TM Perforation things to avoid
Avoid: eardorps containing gentamycin, neomycin, sulfate, or tobramycin
123
TM Perf treatment
Systemic antibiotics if otorrhea, paper-patch method in office, Gelfoam plug, fibrin glue, surgery
124
What is the most common treatment for a TM perf?
Most heal spontaneously- can refer pt if not better in 2 mos, have significant hearing loss or have ossicular trauma
125
Auricular hematoma
Results from direct trauma, shearing forces cause the separation of the anterior auricular perichondrium from the cartilage, hematoma forms
126
Treatment for an auricular hematoma
Early identification: drainage with a needle, I&D, splints, compression
127
Mastoiditis treatment
Consult, medical, surgical
128
How do tongue and lip cancers present?
As exophytic (outward growth) or ulcerative lesions
129
What types of oral lesions should be biopsied?
Persistent papules, plaques, erosions or ulcers
130
What accounts for up to 80% of squamous cell carcinoma of the head and neck?
Tobacco and ETOH
131
Cancer of oral cavity
Associated with ulcers or masses that do not heal
132
What is aphthous stomatitis
Canker sore, painful oral lesions, sometimes genital with repeated development
133
What is the most common acute oral lesion?
Aphthous stomatitis
134
What are the classifications of aphthous stomatitis>
1. Simple aphthous (Mikulicz) | 2. Complex aphthous
135
Simple aphthous
Several episodes a years, lasting up to 14 days, limited to oral mucosa, most common form of disease
136
Complex aphthous
Oral and genital, more numerous lesions, larger than 1cm, 4-6 weeks to resolve, patients almost always have them
137
Ulcer morphology (aphthous stomatitis)
Minor ulcers <1cm major >1cm | Herpetiform 1 to 2 cm typically in clusters
138
Pathogenesis behing aphthous stomatitis
Unknown, likely multifactorial involving immune dysregulation, weak anti-inflammatory response, possible genetic predisposition
139
What diseases can aphthous stomatitis be seen in?
Celiac disease, IBD, Crohns. Diseases that cause decrease in mucosal thickening
140
Risk factors for aphthous stomatitis
Smoking cessation, familial tenency, trauma-dental cleaning, hormonal factors-progestin levels fall in luteal phase of menstrual cycle, emotional stress, HIV
141
Clinical presentation of aphthous stomatitis
1-5, round to oval, clearly defined ulcers, erythematous rim, yellowish central, small 1-3 cm, painful
142
How to diagnose aphthous stomatitis
Hx and PE, history of recurrent self-limited oral ulcers, Bx not needed
143
Management of aphthous stomatitis
Oral hygeine: non alcoholmouth wash and soft toothbursh Pain control: viscous lidocaine applied or swish and spit, Diphenhydramine liquid swish and spit, dyclonine losenges Topical steroids: Dexamethasone elixir swish and spit, Clobetasol gel, Triamcinolone paste
144
Management of complex aphthous stomatitis
Intralesional or glucocorticoids for recalcitrant lesions or sever disease, Colchicine, Dapsone, Pentoxifylline (bronchodilator), Thalidomide in HIV pts
145
Oral leukoplakia is what?
A benign reactive process, significance depends on degree of and presence of dysplasia.
146
What is there an association with?
Oral leukoplakia and HPV
147
Epidemiology of Oral leukoplakia
1-20% progress to carcinoma in 10 yrs, similar to squamous cell carcinoma, common in smokeless tobacco users
148
Clinical manifestations of Oral leukoplakia
Lekoplatic lesions that show up in trauma prone regions (cheek, dorsum of tongue) Thin areas of mucosa, not painful, whitish grey lesions, flat, not well defined, cant scrape off easily*
149
Diagnosis of Oral leukoplakia
Hx and PE, whitish area cant be scarped off that should tip you off, all indurated areas should be biopsied
150
Management of Oral leukoplakia
Most dont need treatment, surgical removal, cryoprobe, recenter interest in chemoprevention, oral retinoids showing promise
151
Oral hairy leukoplakia
Separate from oral leukoplakia, not premalignant, EBV associated, occurs almost entirely in HIV affected patients
152
HSV-1 Herpes
Herpes labialis, effects multiple sites in the body, perioral and oral cavity, HSV 1 causes 80% of oral lesions, 20% of genital lesions
153
Epidemiology of HSV-1
Associated with increasing cases of genital herpes, more common in women, majority are transmitted by people who dont know they have it
154
Pathophys of HSV-1
HSV enters, undergoes latency and can survive in neural ganglia. Prevents elimination by immune response, recurrent infection is common-usually local symptoms only
155
What are the types of infections? (HSV1)
Primary and Secondary
156
What is primary HSV1
Highly variable usually severe, systemic
157
What is secondary HSV1
Common typically less severe, local
158
Clinical manifestation of HSV1
Primary infection: systemic symptoms, usually affects the gingiva. Herpetic gingivastomatitis most common*
159
What do the lesions look like in herpes simplex infection?
Multiple oral vesicular lesions and erosions surrounded by erythematous base, painful
160
Young children with herpes simplex can also have
Fever, LAD, drooling, decreased oral intake
161
Other clinical manifestations of herpes
Prodromal signs of burning, tingling pain 24 hours prior to outbreak, recurrent outbreaks usualyl on lip borders, recurrence may be first indication of infection
162
Risk factors for herpes
Sunlight exposure, stress, trauma
163
How can you diagnose HSV1?
Tzanck smear, immunofluoresence smear or viral cx, unroof th evesicle, serology for HSV by PCR
164
Management of HSV1
Systemic antivirals: Acyclovir, Valacyclovir, Famciclovir Swish and spit miracle mouthwash Supportive, popsicles
165
What involves the mucous membranes- oropharyngeal and esophageal
Oral candida (thrush)
166
Epidemiology of thrush
Young infants, older adults who wear dentures, Abx, chemotherapy, radiation head and neck, immunodeficiency, inhalers, xerostomia
167
Pathogens most commonly causing thrush
Candida albicans, Candida glabrata, Candida krusei, Candida tropicalis
168
Classification of thrush
Pseudomembranous and atrophic
169
PSeudomembranous thrush
Most common form. white plaques on buccalmucosa, palate, tongue and orophyarnx
170
Atrophic thrush
(Denture stomatitis), most common form in older adults. Found under the upper dentures, erythema without plaques
171
Clinical manifestations of thrush
Asymptomatic: dry mouth, loss of taste, pain with swallowing or eating White plaques on buccal mucosa, palate, or tongue, erythema without plaques in denture wearers, painful, beefy red tongue *angular chelitis and painful fissuring*
172
Diagnosis of thrush
White plaques usually removable, fungal Cx, KOH prep, refractory thrush should warrant HIV testing
173
Management of thrush
Local therapy, Nystatin suspension swish and swallow, Clotrimazole troches (lozenges), Miconazole buccal tabs, Diflucan PO
174
What is known as the Red eye
Conjunctivitis
175
Conjunctivitis
Usually benign and self-limited, inflammation of the conjunctiva- injection Thin tissue that lines the insides of lid and top of the globe, generally transparent
176
Classifications fo conjuncitivitis
Bacterial, viral, allergic, traumatic, toxic
177
Bacterial conjunctivitis
More common in children, spread by direct contact, highly contagious
178
Pathogens that cause bacterial conjunctivitis
S. aureus, S. pneumoniae, H. influenzae
179
Clinical manifestations of bacterial conjunctivitis
Red eye usually unilateral, discharge-green, yellow, white. Often complain of eyes stuck shut, itchy, feels gritty like sand
180
More clinical manifestations of bacterial conjunctivitis
Dry crusty stuff at lid margins and corner of eye, purulent discharge
181
What should be done for each eye complaint of bacterial conjunctivitis?
Fluorescein every eye complaint* do Fundoscopy on every eye complaint
182
Management of bacterial conjunctivitis
Erythromycin ophthalmic ointment, Trimetoprim-Polymyxin drops
183
Alternative treatments for bacterial conjunctivitis
Bacitracin ointment, Sulfacetamide ointment, Fluoroquinolone drops good in contact lens wearers
184
Viral conjunctivitis
Usually part of a viral prodrome, patients have sore throat, fever, LAD, pharyngitis, highly contagious, spread by direct contact
185
Which virus commonly causes viral conjunctivitis?
Typical pathogen in adenovirus
186
Clinical manifestations of viral conjunctivitis
Red eye, mucoserous or watery discharge, burning, sandy or gritty feeling, both eyes usually involved in 24-48 hours. New rapid (10 min) test for adenovirus is now available
187
Management of viral conjunctivitis
Self-limited, warm or cool compresses, gets wrorse in first 3-5 days, gradual resolution
188
Allergic conjunctivitis
Caused by airborne allergens that come in contact with the eye, specific IgE cause mast ell degranulation and histamine release Pts have hx of allergies, itchy eyes look for corneal abrasions!
189
Clinical manifestations of allergic conjunctivitis
Bilateral eye redness, itching, grittiness, burning, irritation, watery dc, morning crusting, marked chemosis, infraorbital edema: allergic shiners
190
Management of allergic conjunctivitis
Remove offending agent, wear sunglasses, change filters
191
Managemtn of allergic conjunctivitis (drugs)
Antihistamine/Vasoconstrictor combo: Naphazoline/pheneramine (Naphcon-A) Antihistamines with mast cell stabilizer properties: Olopatadine (Patanol) Mast cell stabilizers: Cromolyn sodium (Optocrom)
192
Glucocorticoids used in allergic conjunctivitis
Loteprednol (lotemax), use carefully, can rise IOP, up to 2 weeks only*
193
Traumatic conjunctivitis
Due to foreign body, treatment is removal
194
Toxic conjunctivitis
Smoke, liquid, fumes, chemicals, akalai and acidic Use litmus paper for pH testing- 7.0 normal 20% of chemical injuries result in significant visual and cosmetic disability
195
Pathophys of toxic conjunctivitis
Acid burns: dissociate into hydrogen ions in cornea, hydrogen damages ocular surface by altering pH, produces protein coagulation, preventing deeper penetration of acids into the eye. Hydrofluoric acid acts as an alkali
196
Common acids in toxic conjunctivitis
``` Battery acids: Sulfuric acid Bleach: sulfurous acid Glass polish: hydrofluoric acid Vinegar: Acetic acid Hydrochloric acid ```
197
Which type of burns are the worst?
Alkali, dissociated into a hydroxyl ion, liquifies the fatty acid of a cell membrane and penetrates cell membrane
198
Common alkalis found in toxic conjunctivitis
``` Ammonia: Cleaning products, fertilizer Lye: drain cleaners Lime: plaster, mortar Airbag rupture: sodium hydroxide Fireworks: magnesium hydroxide ```
199
Management of toxic conjunctivitis
Tetracaine drops, immediate flushing of the eye until pH is normal, use morgans lens for irrigation
200
Conjunctivitis key points
Diagnosis based on hx and exam, hx is important. Fluoroscein and do a fundoscope for every eye patient, ophthalmology referral
201
What is an infection of the anterior portion of the eyelid?
Preseptal/periorbital cellulitis
202
Preseptal/periorbital cellulitis
Doesnt involve the orbit or other ocular structures. Mild condition-rarely leads to complications, can advance to orbital cellulitis
203
Etiology of preseptal/periorbital cellulitis
insect bites, animal bites, foreign body, Dacryocystitis (tear sac inflammation), Conjunctivitis, Hordeolum (stye)
204
What are the common pathogens causing preseptal/periorbital cellulitis
S. aureus, s. pneumoniae, MRSA
205
Clinical manifestations of preseptal/periorbital cellulitis
Ocular pain, eyelid swelling, erythema, warmth
206
Diagnosis of preseptal/periorbital cellulitis
History and PE, CT or MRI, need to distinguish between preseptal or orbital cellulitis
207
Management of preseptal/periorbital cellulitis
Doxycyline: not approved for kids under 8 | Clindamycin PO, Bactrim plus Amox or Augmenting or Cefpodoxime or Cefdinir PO
208
Orbital Cellulitis
Infection involving contents of the orbit: fat, muscles, no globe involvement, more common in children
209
Causes of Orbital Cellulitis
Rhinosinusitis most common, orbital trauma, dacryocystitis, tooth infection, ophtlamic surgery
210
Most common pathogens causing Orbital Cellulitis
S. aureus and streptococci
211
Clinical manifestations of Orbital Cellulitis
Swelling, erythema, warmth, ophthalmoplegia, proptosis, pain with eye movement, diplopia
212
Complications of Orbital Cellulitis
Orbital abscess, subperiosteal abscess, brain abscess, cavernous sinus thrombophlebitis
213
What tools can be used to diagnose Orbital Cellulitis?
Confirmed with a CT or MRI
214
Management of Orbital Cellulitis
Vancomycin plus Ceftriazone or Cefotaxime or Bactrim or Zosyn
215
When should we start to see symptoms improvement for Orbital Cellulitis?
24-48 hours, if no improvement surgery sholdl be considered
216
Herpes Keratitis
Corneal infection and inflammatoin
217
What is a major cause of blindness from corneal scarring?
Herpes keratitis
218
How is herpes keratitis spread?
Direct contact with mucous membrane
219
Classification of herpes keratitis
1. Infectious epithelial keratitis 2. Stromal keratitis 3. Endotheliitis 4. Neurotrophic keratopathy
220
Stromal keratitis
Viral infection of the stroma
221
Endotheliitis
Immune reaction
222
Neurotrophic keratopathy
Cornea hypesthesia from damage to the optic nerve
223
Epidemiology of herpes keratitis
Endemic in humans, incubation is 1-5 days. Majority of cases are unilateral*
224
What three processes are involved in herpes keratitis?
1. Active infection 2. Inflammation caused by infection 3. Immune reaction
225
What is the result in herpes keratitis?
Structural changes in the cornea
226
Clinical manifestations of Herpes keratitis
Pain, visual burning, tearing
227
How can we diagnose herpes keratitis?
Conjunctival infection, dendritic lesions on fluorescein*
228
Management of herpes keratitis
Topical antiviral agents: Trifluridine, Ganciclovir, Acyclovir Oral agents: Valacyclovir, Famcyclovir, Ganciclovir
229
What are meibomian glands?
Inside rim of eyelids, 50 on upper lid and 25 on lower lid.
230
What is the function of the meibomian glands?
Sebaceous glands that secrete oily substances to keep the eye lubricated. Prevents the evaporation of tears and dysfxn leads to dry eyes
231
What is blepharitis?
Chronic eye condition characterized by inflammation of the eyelids with intermittent exacerbations
232
What are the two types of blepharitis>?
Anterior and posterior blepharitis
233
Which type of blepharitis is more common?
Posterior
234
Anterior blepharitis
Inflammation at the base of the eyelids, more likely in young and female
235
What are the two variants of anterior blepharitis?
Staphylococcal and Seborrheic
236
Pathophys of anterior blepharitis?
Staph colonization of eyelids, possibly due to direct infection, reaction to staph exotoxin, allergic response to staph antigens
237
Clinical manifestations of anterior blepharitis
Eyelid edges pink irritated swollen with crust, malposition of eyelids in chronic cases. eyelashes may be misdirected, thinning. Diffuse conjunctival injection
238
Posterior blepharitis
More common, associated with skin conditions like rosacea and seborrheic dermatitis
239
Pathophys of posterior blepharitis
Inflammation of meibomian glands, causes dysfxn and altered secretions. Increase in: free fatty acids, unsaturated fatty acids and an impaired lipid layer of tear film
240
Clinical manifestations of posterior blepharitis
Red eyes, gritty sensation, burning, excessive tearing, itchy eyelids, red swollen eyes, crusting, flaking eyelid skin, photophobia, blurred vision
241
Diagnosis of blepharitis
No confirmatory diagnostics or lab tests. Want to distinguish between ant and post
242
What are the differences when diagnosing anterior vs posterior blepharitis?
Anterior has the base of eyelash swelling, redness, crust and posterior has the meibomian gland enlargement, plugging with waxy secretions
243
Management of blepharitis
Counseling, alleviate acute sx, warm compresses, lid massage, lid washing, artifical tears
244
What topical ointments or drops can be used for blepharitis?
Azithromycin, Erythromycin, Bacitracin (more effective with anterior) Oral tetracycline or Doxycyline 2-4 weeks for severe or chronic cases
245
What is a hordeolum?
Stye. Acute, purulent inflammation of the eyelid. May be sterile or show bacteria
246
What is the most common pathogen that causes hordeolum?
Staph
247
Internal hordeolum
Infection of meibomian glands at the conjunctival side
248
External hordeolum
Infection of eyelash follicle at the lid margin
249
What is the management of a hordeolum
Warm compresses, topical abx, may harden to a chalazion
250
Chalazion
Chronic inflammatory lesions due to blockage and swelling of meibomina glands of eyelid
251
When is chalazion commonly seen?
In patients with eyelid margin blepharitis and rosacea
252
Epidemiology of chalazion
More common in adults 30-50. Can start out red, tender, swollen then becomes a painless and larger, rubbery nodular lesion
253
Is a chalazion due to an infection?
No
254
Treatment of chalazion
Minimal, usually self-limiting. Can take a few weeks to a month. Use warm compresses, eyelid massage
255
What can you do if the chalazion is non-resolving?
Refer them to an ophthalmologist for I&D or give a glucocorticoid injection
256
Ectropion
Lower eyelid is rolled out, sagging of the eyelid leaves the eye dry, exposed, and irritated
257
Etiology of ectropion
Aging: connective tissue sagging, facial nerve paralysis: Bells palsy, stroke, trauma or scarring, certain dog breeds
258
Clinical manifestations of ectropion
Wet inner conjunctiva is exposed and visible, excessive tearing, chronic inflammation, redness, gritty feeling, dry eye, crusting, multiple infections
259
Management of ectropion
Temporary: Artifical tears, ointments to lubricate the eye Permanent: Surgery, incision of skin of outside corner to shorten and tighten the lower lid
260
Entropion
Eyelid rolls inward toward the eye, eyelashes rub against the conjunctiva, chronic irritation
261
Etiology of entropion
Aging and weakening of certain muscles, trauma, scarring, surgery
262
Clinical manifestations of entropion
Red eyes, irritated, gritty sensation, tearing, mucous discharge, photophobia. Lower eyelid rolled in, absent eyelashes, corneal abrasion
263
Management of entroption
Temporary: Artificial tears Permanent: Tightening of the eyelid and its attachments to restore eyelid position
264
Dacryadenitis
Inflammation of the lacrimal glands, most commonly caused by bacterial or virus
265
What can cause dacryadenitis?
Viral, bacterial, fungal, inflammatory
266
What are the bacterial pathogens that can cause dacryadenitis?
Staph aureus, strep, n. gonorrhea, treponema, m. tuberculosis, chlamydia, borrelia burgdorferi
267
What are the viral pathogens that can cause dacryadenitis?
Mumps, EBV, coxackie, herpes zoster, mono
268
What are the fungal pathogens that can cause dacryadenitis?
Histoplasmosis, Blastomycosis, Pasaties, Protozoa
269
What inflammatory conditions can cause dacryadenitis?
Sarcoidosis, Graves, Sjogrens
270
Clinical manifestations of acute dacryadenitis
Unilateral, severe pain, redness, swelling, supraorbital pressure, rapid onset. Conjunctival swelling and redness, discharge, erythema of entire eyelid, submandibular LAD, exopthalmos, ocular motility restriction
271
Clinical manifestations of systemic dacryadenitis
Fever, parotid gland enlargement, URI, malaise
272
Clinical manifestations of chronic dacryadenitis
Usually bilateral, painless enlargement, present more than a month, more common than acute
273
To diagnose dacryadenitis
Lacriam gland often enlarged and easily seen with eversion of upper eyelid. Can do a CT of the orbits with contrast
274
Management of dacryadenitis
Viral: self-limiting, supportive Bacterial: Keflex (1st gen ceph) Protozoal or fungal: Antifunal or antiamoebic Inflammatory: Investigate for systemic causes and treat accordingly
275
Dacryostenosis
Nasolacrimal duct obstruction, most common cause of persistent tearing in infants
276
Dacryostenosis treatment
Massage, lacrimal duct probing. Spontaneous resolution by 6-12 months of age
277
Keratoconjunctivitis Sicca
Dry eyes, multifactorial disease of the tears and ocular surface. Results in ocular discomfort and vision impairment
278
Epidemiology of Keratoconjunctivitis Sicca
Difficulty defining disease, lack of confirmatory diagnostic test, more prevalent in women
279
What do the tear films consist of in Keratoconjunctivitis Sicca
Aqeous mucous an dlipid components
280
Any dysfxn of what can lead to dry eyes?
Lacrimal functional unit: eyelids, lacrimal glands, eye surface
281
What are the two classifications of Keratoconjunctivitis Sicca
Decreased tear production | Increased evaporative loss
282
Decreased tear production (Keratoconjunctivitis Sicca)
Lacrimal gland dysfxn or destruction Sjogren syndrome: systemic autoimmune inflammatory infiltration of the lacrimal glands. Leads to cell death and hyposecretion
283
Lacrimal dysfunction without systemic findings can be classified as what?
Non-Sjogrens
284
Increased evaporative loss (Keratoconjunctivitis Sicca)
Excessive water loss form ocular surface, meibomian gland dysfxn, decreased blind function, structural abnormalities of the eyelid, eye drops, chronic contact wearing, ocular allergy syndrome
285
Clinial manifestations of Keratoconjunctivitis Sicca
Dryness, redness, irritaiton, gritty sensation, excessive tearing, photophobia, blurred vision
286
Diagnosis of Keratoconjunctivitis Sicca
Fluorescein stain, Tear break-up time, Schirmers test (# tears produced by each eye), Corneal sensation, tear hyperosmolarity
287
Management of Keratoconjunctivitis Sicca
1st line: Artificial tears** they contain cellulose to maintain viscosity
288
What else can be used to treat Keratoconjunctivitis Sicca
Topical Cyclosporine (restasis), Xiidra-integrin antagonist, Sodum Hyaluronate, Topical glucocorticoids, autologous serum tears, tear stimulation, vitamin A, punctal occlusion, scleral contact lenses
289
What are the organs for body movement?
Semicircular canals
290
Organ for hearing
Cochlear
291
The information from the vestibular labyrinth is relayed via CNVIII to
1. Cerebellum 2. Ocular nuclei 3. Spinal cord
292
What part of the semicircular canal detects when the head tilts down towards the shoulder?
Posterior
293
What part of the semicircular canal detects when the head shakes side to side in "no" motion?
Lateral
294
What part of the semicircular canal detects when the head nods up and down in "yes" motion?
Superior
295
The otolith organs sense what?
Gravity and linear acceleration
296
Utricle registers accelerations in the what plane?
Horizontal, its horizontal in the head
297
Saccule resgisters accelerations in the what plane?
Vertical, vertical in the head
298
CN VIII
Vestibulocochlear Nerve (AKA auditory nerve)
299
Which nerve is responsible for balance and orientation in space and auditory function?
CN VIII Vestibulocochlear
300
What is the length of the eustachian tube?
36-38 mm in adults, children are shorter
301
What is the function of the eustachian tube?
Provides ventilation and drainage for the middle ear cleft
302
Is the eustachian tube usually open or closed?
Normally closed, open only during swallow/yawning
303
What happens when the eustachian tube gets compromised?
Air trapped in the middle gets absorbed creating negative pressure TM retraction
304
Some other normal functions of the eustachian tube include
Equalizing pressure across TM, protecting middle ear from infection and reflux of nasopharyngeal contents, clearance of middle ear secretions
305
What are the two most common ways the ET (eustachian tube) can be blocked?
Allergic response, URI | others: sinusitis, chronic otitis media, congenital or acquired stenosis, neoplasms
306
The failure of ET opening is generally due to what?
Functional or anatomic obstruction
307
Eustachian Tube Dysfunction
Impaired protective function, Impaired clearance, Pressure dysregulation
308
What happens when the ET has impaired protective function?
Reflux of nasopharyngeal pathogens into the ET
309
What happens when the ET has imapried clearance?
Loss of mucociliary function contributing to the inability to clear pathogens
310
What happens when the ET has pressure dysregulation?
Fails to open to allow ventilation
311
What is dilatory dysfunction of the ET?
The tube does not dilate due to: inflammation, pressure dysregulation, acquired anatomic abnormalities
312
What is patulous dysfunction of the ET?
Valve incompetency leads to chronic patency (stuck open)
313
Clinical presentation of ET dysfunction
"Fullness" in the ear, mild-mod decrease in hearing, "popping" sound can be heard from swallowing or yawning, ear pain
314
Physical exam findings of ET dysfunction
Retracted TM on affected side, decreased TM mobility
315
What is the hallmark presentation of dilatory ET dysfunction?
Accompanying symptoms of hearing loss and abnormalities of the tympanic membrane like: retraction and middle ear effusion
316
What will be seen on the otoscopic exam when looking at dilatory ET dysfunction?
Effusion, scarring, thickening of TM TM may also have: retractions, effusions, cholesteatomas, perforations, tympanosclerotic plaques, Weber test can show conductive hearing loss
317
What is the hallmark presentation of patulous ET dysfunction?
"Autophony" patient hears own voice amplified, the symptoms fluctuate, worsened by exercise and prolonged speaking, ear fullness
318
Physical exam findings of patulous ET dysfunction
Breathing induced excursions )movements) of the TM, sensorineural hearing loss
319
What is the treatment for dilatory ET dysfunction?
Treat underlying etiology with: antihistamines, decongestants, nasal steroids, valsalva
320
What is the treatment for patulous ET dysfunction?
Treat if severe symptoms >6weeks, ventilation tubes in severe cases
321
What else can you do for someone with an ET dysfunction?
Refer to ENT! Nasal endoscopy, audiology studies, CT or MRI w/contrast if >3mos of symptoms or with middle ear effusion, surgery (tubes), balloon dilatation
322
What is vertigo?
Symptom of illusory movement, described as sensation of motion when there is no motion, or an exaggerated sense of motion in response to movement
323
What is the key to diagnosis of vertigo?
Duration of episodes and association with hearing loss
324
Peripheral and central vertigo symptoms are caused by what?
Vestibular damage/dysfunction
325
Peripheral vertigo involves which organs?
Semicircular canals, otolith organs
326
Onset of peripheral vertigo?
Sudden, often associated with tinnitus and hearing loss, horizontal nystagmus may be present
327
Central vertigo involves what organs?
Cerebellum, CN VIII, brainstem
328
Onset of central vertigo?
Gradual, no associated auditory symptoms
329
Etiology of peripheral vertigo
Benign Paroxysmal Positional Vertigo (BPPV), Vestibular neuritis (Labrythititis), Meniere's Disease, Herpes zoster oticus (Ramsey Hunt), Acoustic neuroma, Aminoglycoside toxicity, Superior Semicircular Dehiscence Syndrome
330
Etiology of central vertigo
Migraines, Cerebral tumor on CN VIII, Chiari malformation, brain ischemia (cerebllar infarct and hemorrhage), TIA, MS
331
What drugs are ototoxic?
Aminoglycosides, Antidepressants, anxiolytics, furosemide, amiodarone, ASA
332
Clinical presentation of vertigo KEYS
Duration and Hearing loss
333
Nystagmus
Uncontrolled movement of the eyes, reflex to adjust for slight movement of head and help stabilize and sharpen an image
334
Tinnitus
Perception of sound int he absence of an external source, usually buzzing, ringing, or hissing in 1 or both ears
335
Benign paroxysmal position vertigo (BPPV)
Provoked by specific head movements: turning in bed, tilting head backward to look up
336
What is BPPV caused by?
Calcium debris in semicircular canals (posterior canal most common)
337
BPPV Symptoms
Vertigo sensation: short in duration (seconds to minutes), ear pain hearing loss and tinnitus are all ABSENT
338
BPPV Clinical presentation
Rapid onset of dizziness or spinning, nystagmus (clockwise, rotary nystagmus)
339
Nystagmus in BPPV
Fatigable, with Dix-Hallpike testing. Typically the sensation of motion precipitated by sudden head movements of moving the head in certain way, N/V also common
340
BPPV Diagnostics/Testing
Dix-Hallpike positional testing: 5-15 sec between supine positioning and onset of nystagmus. Induces vertigo/spinning nystagmus
341
Further testing for BPPV if needed
Electronystagmography: records eye movements. MRI/CT to rule out other causes
342
BPPV Treatment with pharmacotherapy
Symptomatic tx, self-revolving within months. Can use antihistamines, antiemetics, BZDs, Scopolamine patch
343
BPPV vestibular rehab
Gaze stimulation exercises, repositioning maneuvers (Epley Maneuver), surgery (only after 6 mos, very rare)
344
Labrynthitis (Vestibular Neuritis)
Viral or postviral inflammatory disorder, affecting the vestibular portion of CN VIII Vesitublar neuritis -> vertigo w/o hearing loss Labrynthitis -> vertigo w/unilateral hearing loss
345
Clinical presentation of vestibular neuritis
Rapid onset of sever, persistent vertigo, N/V, gait instability, decreased hearing in 1 ear in Labrynthitis, horizontal nystagmus, +head thrust, if patient falls -> toward the affected side
346
Imaging for vestibular neuritis
MRI/MRA for infarct, CT if MRI/A not available
347
Treatment for vestibular neuritis
Corticosteroid therapy, symptomatic treatment: antihistamines, antiemetics, vestibular rehab
348
Meniere's Disease
Peripheral vestibular disorder attributed to excess endolymphatic fluid pressure
349
What does Meniere's disease cause
Episodic inner ear dysfunction "labyrinthine hydrops"
350
What parts of the ear are affected in Meniere's?
Cochlea, semicircular canals, otolithic organs
351
What are some risks associated with Meniere's?
Allergy, stress, viral
352
Clinical presentation of Meniere's
Vertigo, sensorineural hearing loss, tinnitus. Episodes are unpredictable, can last hours, be recurring, and are followed by fatigue
353
How long can the symptoms last for in Meniere's?
Spontaneous- 20 min-24 hours, 6-11 attacks per year
354
Symptoms of Meniere's
Unilateral sensorineural hearing loss, tinnitus, fullness/pressure in the ear, N/V, disabling imbalance, horizontal-torsional nystagmus seen during acute attack
355
Imaging for Meniere's diease
Audiometry: low frequency sensorineural hearing loss Electronystagmography: Unlitearly reduced vestibular response Caloric testing: often shows loss/impairment of thermally induced nystagmus on affected side. MRI, lab and RPR to rule out others
356
Vestibular testing for Meniere's (results)
ENG abnormal on affected side, rotatory chair test, computerized dynamic posturography
357
Audiometry testing for Meniere's
If low frequency sensorineural hearing loss -> helps confirm
358
Caloric testing for Meniere's
This is an otoneurolgic evaluation of the status of the vestibular-ocular reflex. Put cold then warm water into ear, nystagmus will appear
359
COWS
Cold opposite, warm same (test for meiniere's)
360
Meniere's treatment
Reduce frequency and severity of vertigo attacks, eliminate hearing loss and tinnitus, minimize disability, prevent disease progression
361
Acute symptom treatment for Meniere's
Antihistamines, antiemetics, BZDs, anticholingerigcs
362
Long-term symptom treatment for Meniere's
Lifestyle adjustment, salt restriction, limit caffeine and nicotine, limit alcohol, if tinnitus avoid excessive noise
363
Procedural treatments for Meniere's
Surgical: succulotomy, intratympanic glucocorticoids, positive pressure pulse generator, intratympanic gentamicin injection, surgical labyrinthectomy, vestibular nerve resection
364
Minors Syndrome
Also called Semicircular Canal Dehiscence Syndrome
365
Semicircular Canal Dehiscence Syndrome
Thinning of bone that separates the superior semicircular canal from middle cranial fossa, allowing pressure to be transmitted to inner ear
366
Symptoms of Semicircular Canal Dehiscence Syndrome
Vertigo provoked by coughing, sneezing, Valsalva, nausea, hearing loss in some pts
367
Semicircular Canal Dehiscence Syndrome can be tested how>
cVEMP: cervical vestibular evoked myogenic potential
368
Pulsatile tinnitus etiology
Listening to won heartbeat, vascular disorders, arteriovenous shunts, venous hums, ET dysfunciton, arterial bruits
369
Non-pulsatile tinnitus etiology
Clicking tinnitis, secondary to middle ear spasm, unilateral
370
Tinnitus etiology other
Ototoxic meds, presbycusiss (sensorineural loss with aging),
371
What is a Chiarai malformation?
low lying cerebellar tonsils cause tension on auditory nerve
372
What is otosclerosis?
abnormal bone repair of stapes footplate bone
373
Diagnosis/Imaging for tinnitus
Audiometry to R/O associated hearing loss, MRI if unilateral especially with hearing loss to R/O retrocochlear lesions (Vestibular schwannoma)
374
Tinnitus treatment
Avoid excessive noise, treat underlying depression and insomnia, cochlear implants, retraining therapy