TRANS 46 - 48 Diseases of the external, middle and inner ear Flashcards
The tympanic membrane is an extremely thin 3-layered
membrane which is semi-transparent
These 3 layers are the
squamous, fibrous and mucosal layers
Tympanic membrane is also divided into 2 parts. The
pars
tensa and pars flaccida.
is the lateral boundary of the epi-tympanum
pars flaccida
is the lateral boundary of the meso-tympanum
pars tensa
The external auditory canal (EAC) is roughly 20mm and is
divided into
the outer 1/3 cartilaginous portion and the 2/3
bony portion
The junction between the cartilaginous and bony portion is
called the___________ which is the narrowest portion of the
canal.
isthmus
So the anterior wall, you will find a two openings, the opening of the
the opening of the tensor tympany muscle and the opening of the eustachian tube.
The roof consists of a thin plate of bone which is the ____________, which separates the middle ear from the medial cranial fossa or the brain.
tegmen tympani
This is also called the Mastoid wall of the middle ear. You will find indentations from the semicircular canal and also from the facial nerve.
You will also see the pyramidal eminence.
POSTERIOR WALL OF THE MIDDLE EAR
At the superior portion of the mastoid wall, you will find a opening which is a communication from the mastoid air cells and the middle ear, and this opening is called
the aditus to the mastoid anguim.
First we determine if there is hearing loss then after that we determine what kind is it. mild moderate severe profound?
Mild (25-40 dB), Moderate (41-70 dB), Severe (71-90 dB), profound hearing loss (>90 dB).
Produced by glandular structures, sebaceous and apocrine glands located in the cartilaginous portion of the EAC.
Cerumen
This is simply called pimple
• Otits externa circumscripta
• Confined to the fibrocartilaginous portion of the EAC (external auditory canal)
Furuncolosis
- Begins in the pilosebaceous follicle
- Caused by Staphylococcus aureus
- Abscess formation
FURUNCULOSIS
manifestations of furunculosis?
• Manifestation: ear pain, ear blockage, ear discharge
Treatment of furunculosis?
Treatment: topical medications (mupirocin), heat, analgesic
I would usually prescribe oral antibiotic which is co-amoxiclav 3 times a day for 7 days and I’ll instruct patients to apply Bactroban in this area, then heat to warm this area with a pouch/compress bag for 15 mins 3 times a day for 5 days.
Usually this will cause continuous drainage of the abcess for 2-3 days after that there will be a relief from the pain and discontinue the medication
Also known as “swimmer’s ear”. Diffuse = it involves the whole part of the external auditory.
• Occurs during hot, humid weather. When people go for swimming.
• Caused by Pseudomonas and less often by S. aureus, E. coli, Enterobacter.
DIFFUSE OTITIS EXTERNA
manifestation of diffuse otitis externa
Manifestations: tragal tenderness, severe ear pain, canal wall swelling involving most of the canal, scanty discharge, normal or slightly diminished hearing, absence of fungal, lymphadenopathy.
If you press the tragus, you will elicit pain.
Treatment of Diffuse otitis externa
Treatment: otic drops
In the market we prescribe this and it composed of fluocinolone poly mixin and neo-mixin. 3 drops 3 times a day for 7 days. Sometimes we add oral antibiotic
• Caused by fungus most commonly, Pityrosporum and Aspergillus; occasionally, Candida.
• Manifestations: Ear itch, ear pain, ear blockage.
Its very itchy and very painful at the same time.
OTOMYCOSIS
treatment otomycosis
Treatment: Suctioning, aural toilette (put hydrogen peroxide), topical antifungal agent, boric acid, acetic acid.
Aural toilette – put hydrogen peroxide 1 part to the ear for one minute and tilt it to the opposite side then drain and put topical antifungal.
Clotrimazole 3 drops to the ear 2 a day for 7 days. And follow up after 1 week to check because this is a fungal infection.
Ramsay hunt Disease
• Viral infection of the geniculate ganglion.
Herpes zoster oticus
Manifestation of herpes zoster oticus?
Manifestation: facial paralysis otalgia, vesicular skin lesion involving portion of the external ear
Pathognomonic sign of herpes zoster oticus?
We would see rashes in the ear and this is pathognomonic. This are lesions that are vesicular in nature and involving the pinna, sometimes at the auditory meatus.
It is a swelling in the pinna that involves the perichondrium
which is the sheet covering the cartilage.
In between the perichondrium and the cartilage there is an
accumulation of fluid. There is inflammation and various
bacterial infections.
• Inflammation of the perichondrium.
• Caused by effusion or pus between the perichondrium and
cartilage.
• Commonly develops after trauma.
PERICHONDRITIS
Causative agents of perichondritis?
Causative agents:
o Staphylococcus
o Streptococcus
o Pseudomonas
manifestations of perichondritis
o Ear swelling, redness, tenderness, and warmth
Treatment of perichondritis?
o Topical antibiotic (ofloxacin oral + mupirocin ointment)
Usually ofloxacin 200mg tablet twice BID for 7 days and
mupirocin application BID for 7 days.
If there is obvious abscess formation it can be drained.
• Unknown etiology
• Inflammation and destruction of cartilage.
• Generalized disorder of the cartilage (mostly nose and ears)
• Floppy ears; saddle-nose deformity.
Due to the destruction of the cartilage.
• Alteration of inflammation between the two ears.
• Disease activity fluctuates.
• Single or multiple occurrences.
• Treatment is use of steroids for acute attacks
REPLASING POLYCHONDRITIS
The cartilage is not sutured, only the skin is sutured
\true or false?
True
• Pinna is susceptible because of its location.
• Exposure to very low temperatures causes a severe and
prolonged vasoconstriction of the capillary walls.
• The loss of sensation allows a significant amount of damage
to occur without the individual’s knowledge.
• The ear becomes red, swollen, and tender.
FROSTBITE
treatment of frostbite?
• Treatment is it should be warmed with sterile dressing.
o Antibiotics and analgesics and debridement.
The gangrenous portion is removed and usually, it heals by itself. Complete healing is usually at around 6 weeks.
- A very aggressive for of otitis externa.
- Typically seen in elderly people and those who are immunocompromised like people with diabetes.
- Potentially lethal infection of the auditory canal, surrounding tissue and skull base.
NECROTIZING (MALIGNANT) OTITIS EXTERNA
etiology of necrotizing malignant otitis externa
• For the etiology, the most common pathogen is Pseudomonas aeruginosa.
these are s/sx of what?
o Spread of infection from external auditory canal to bone (ostitis).
o Replacement of compact bone with granulation tissue.
o Spread to skull base
o Facial nerve paralysis and cranial nerves IX, X, and XI palsies.
o Typical symptoms are severe otalgia, granulation tissue in the meatus and tactical nerve paralysis.
NECROTIZING (MALIGNANT) OTITIS EXTERNA
Tx of necrotizing (malignant) otitis externa
Treatment requires prompt hospitalization, treatment of diabetes, use of high-dose intravenous antibiotics specific for Pseudomonas, and sometimes surgery.
Surgical removal of the affected portion, the eroded portion, so that it will discontinue the further inflammation and infection of the surrounding tissues.
Grading of ear malformations?
Grade 1- smaller thatn normal but has normal anatomy
Grade 2- part of the ear looks normal, usually the lower half. the canal may be normal , small or completely closed
Grade 3 - just a small remnant na peanut shaped skin and cartilage. there is no canal - aural atresia
Grade 4 - complete absence of both the external ear and the canal. aka anotia
Benign tumor
o Solitary, firm, rounded growth attached by a small bony pedicle.
osteotoma
o More common
o Multiple and bilateral
o Associated with swimming in cold waters.
o Hypertrophic canal bone
exostosis
o Most common malignancy of the external ear canal.
(Figure 11) a malignant growth in the helix of the pinna.
Usually starts as a non-healing wound that the patient keeps scratching until there is inflammation that becomes chronic until it ulcerates.
The mass is excised and is submitted for histopathological analysis.
The definitive management is the removal along with 1cm of normal tissue around it. At times the patient is subjected into radiotherapy to prevent recurrence.
Squamous cell carcinoma
• Tubotympanic inflammation
Tubo- meaning the eustachian tube.
• Non-infectious
• Presents with ear fullness and hearing loss, usually without otalgia.
• Disorder of ventilation and drainage of the middle ear.
• Mainly seen in children (dual peak age of 2 and 5 years).
OTITIS MEDIA WITH EFFUSION
• Pathogenesis
o Eustachian tube dysfunction.
o Poor ventilation of the middle ear cavity.
o Resorption of the air in the middle ear.
o Vacuum (hydrostatic pressure differences)
o Transudation of plasma from blood vessels.
what disease?
OTITIS MEDIA WITH EFFUSION
Etiology is eustachian tube dysfunction.
Swelling of eustachian tube mucosa (allergy).
o Obstruction of eustachian tube ostium (hypertrophic adenoids).
o Does not open on swallowing.
OTITIS MEDIA WITH EFFUSION
Pathognomonic sign of OTITIS MEDIA WITH EFFUSION
Diagnosis
o Presence of bubbles in the middle ear.
Very pathognomonic.
Dull tympanic membrane on otoscope
three most common causative agents of acute otitis media?
The three most common etiologies are:
o Streptococcus pneumoniae (Most common)
o Hemophilus influenzae
o Moraxella catarrhalis
Stages of acute otitis media
• Stages o Hyperemia o Exudation o Suppuration o Coalescence
2 types of chronic otitis media?
• Two types
o Chronic Mesotympanic Otitis Media
o Chronic Epitympanic Otitis Media with otitis and cholesteatoma
o Tybo-tympanic type / safe
o Commonly a consequence of AOM when TM2 perforation does not heal and becomes permanent
We usually tell patients if there is perforation to wait for 6 months, after that if the patient still has perforation, then it is already permanent.
o Recurrent infection
Because of the perforation
CHRONIC MESOTYMPANIC OTITIS MEDIA
Causative agents of CHRONIC MESOTYMPANIC OTITIS MEDIA
o Causative organisms: ▪ Pseudomonas sp., ▪ Proteus sp., E. coli, ▪ Staphylococcus, ▪ anaerobes
o Attico-antral type/ unsafe
o Characterized by retraction pocket, cholesteatoma and granulation
o Retraction pocket theory
CHRONIC EPITYMPANIC OTITIS MEDIA WITH OTITIS AND CHOLESTEATOMA
This theory claims that the precursors to cholesteatoma are retraction pockets of the pars flaccida.
Retraction pocket theory
• Infectious invasion of the sigmoid invasion
• Small fragments of thrombus break off
• Clinical features
o Fever - first sign; “picket fence* (spiking)
o Pain over posterior part of the mastoid - Griesinger’s sign
o Papilledema-fundoscopy: blurting of disc margins
Lateral sinus thrombophlebitis
Treatment of lateral sinus thrombophlebitis
- treatment: surgical
- Removal al the focus of infection
- Drainage of the sinus
- Ligation of the internal jugular vein
- Most important and most common tumor of the middle ear and mastoid
- Originates from glomus bodies in the jugular bulb/Jacobson’s nerve
- Benign highly vascular tumor
GLOMUS JUGULARE / GLOMUS TYMPANICUM
Symptoms of Clomus jugulare/ glomus tympanicum
Symptoms:
o Ear fullness
o Conductive hearing loss
o Pulsatile tinnitus
- PE Findings: Bulging purplish mass in the floor of the middle ear
- Brown’s sign: Blanching with pressure from a pneumatic otoscope
- Imaging used for diagnosis: MRI or CT scan
- Treatment: Gamma knife radiosurgery
what dse entity?
GLOMUS JUGULARE / GLOMUS TYMPANICUM
Blanching with pressure from a pneumatic otoscope
Brown’s sign
Most common malignant tumor of the temporal bone is
Squamous Cell Carcinoma
longitudinal vs transverse fracture?
- Longitudinal fracture - run parallel to the long axis of the petrous pyramid; extends from squamous temporal bone to foramen lacerum
- Transverse fractures - run at right angle to the long axis of petrous pyramid; involves otic capsule (cochlea and vestibule)
More common is longitudinal fracture, 80% of the time, usually a result of ________ to the head producing hearing loss and mild vertigo, temporary facial nerve paralysis
lateral blow
Transverse fractures seen in 20% of the time, usually result of __________, accompanied by sensorineural hearing loss, severe vertigo because of otic capsule destruction. Facial nerve paralysis more common”
frontal blow
Michel’s deafness
total lack of development of the inner ear
Mondini’s deafness
with only 1 1/2 turns of the cochlea (instead of 2 1/2)
eplacement of normal bone with spongiotic or sclerotic new bone.
• It is a common cause of progressive hearing loss
Affected is the oval window or foot plate of the stapes”
• Epidemiology - more common in white population; Female > Male
• Etiology - unknown
• Pathophysiology - sclerotic bone causes fixation of stapes
• Clinical feature - Conductive hearing loss; patients have soft speech / can hear their voice louder
Otosclerosis
Conductive Hearing Loss pattern. There is a dip in 2k Hertz (arrows above the line) of the bone conduction; that is
Carhart notch which is pathognomonic of Ostosclerosis”
Treatment for otosclerosis
• Treatment: Stapedotomy
We place a piston in the foot plate of the stapes to connect to the incus”
We remove the supra structure of stapes and afterwards, we create a hole in the footplate and place the prosthesis. Now you have continuous vesicular chain that will transmit sound energy going to cochlea.”
- A benign brain tumor, usually unilateral
- Originates from the Schwan cells of the vestibular nerve / Vestibular Schwannoma
- Mostly affects 40-60 years old
- Predisposing factor: exposure to radiation
- Bilateral acoustic neuromas patients w/ neurofibromatosis II
ACOUSTIC NEUROMA
Diagnosis
• Pure tone audiometry will reveal unilateral/asymmetric sensorineural hearing loss
• Speech audiometry shows poor speech discrimination disproportionate to the hearing loss
• MRI with gadolinium contrast to image the internal auditory meatus (confirmatory)
what disease?
Acoustic neuroma
- Hearing loss associated with aging
- Manifested by 5th - 6th decade of life and slowly progress
- Usually bilaterally symmetrical
- Diagnosis - thru pure tone audiometry: down-sloping (more marked in the higher frequencies)
. PRESBYCUSIS
• Tendency of certain therapeutic agents to damage the inner ear
ototoxicity
• Common ototoxic drugs:
Aminoglycosides, loop diuretics, salicylates, Quinine, Cisplatin
Clinical features of ototoxicity?
- Tinnitus: most common first symptom
- Hearing loss - usually permanent: high-pitched initially
- Balance disorder -rare
- Hearing loss associated with noise exposure
- Temporary or permanent
- Long-term repeated exposure to loud noise (occupational)
- Single-episode exposure to intense loud sounds (blasts) - acoustic trauma
- Potential genetic susceptibility
- Pathophysiology - not entirely clear; apoptosis and necrosis of Outer Hair Cells in the cochlea
- Diagnosis - pure tone audiometry
- Prevention- hearing protective devices (ear plugs and muffs): hearing a
NOISE INDUCED HEARING LOSS
Sensorineural hearing loss of >30=db in >=3 frequencies in <3 days.
• Etiology - 95% unknown
• Clinical Features : Acute onset of hearing loss in one ear
• Diagnosis : Pure tone audiometry & MRI
• Treatment: Steroids + Acyclovir
SUDDEN SENSORINEURAL HEARING LOSS
- Common clinical problem
- Episodes of spinning sensation associated with head movement
- Duration <1min
- Pathophysiology: dislodgement of otoconia from utricle to the SCC
BENIGN PAROXYSMAL POSITIONAL VERTIGO
Diagnosis: of BPPV?
• Diagnosis: Positive Dix-Hallpike test
how to do dix hallpike test?
The patient sits and the doctor turns his head in 45 degree angle and bring the patient swiftly to head hanging position in 30 degree angle and look for nystagmus or if the patient tells he is dizzy: that’s a postiive Dix Hallpike test.”
Treatmetn BPPV?
• Treatment: Epley Maneuver
A maneuver wherein we just reposition the dislodged otoconia back to utricle”
• A disorder of swelling in the endolymphatic space
• Endolymphatic hydrops
o Swelling causes rupture of Reissner’s membrane
o Mixing of endolymph and perilymph
Swelling causes rupture of the membrane, there is mixture of endolymph and perilymph”
Meniere’s disease
Triad of meniere’s
Classical Triad:
- Hearing loss
- Tinnitus
- Vertigo (lasts >1min - hours)
• Sudden onset of severe vertigo which lasts for days to weeks
• Etiology is unknown; probably viral
• Preceded by viral URTI
• Clinical Features:
o Acutely unwell
o patients prefer to lie still on bed for several days
o associated nausea and vomiting
o hearing is normal
• Diagnosis: based on history
• Treatment: Vestibular sedatives (diazepam); steroids; Vestibular rehabilitation
VESTIBULAR NEURONITIS
Infectious; traumatic; complication of otitis media
• Clinical features:
o Symptoms similar to vestibular neuronitis
o With additional sensorineural hearing loss
LABYRINTHITIS
is the drug we usually use for patients having vertigo”
Betahistine
Betahistine is the drug we usually use for patients having vertigo”
Betahistine 24mg BID, for 2 weeks up to months
