Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2017 EENT Clin Med Group > PANCE PEARLS-Hearing, Vestibular, Middle Ear COPY > Flashcards

PANCE PEARLS-Hearing, Vestibular, Middle Ear COPY Flashcards

1
Q

Sensorineural Hearing Loss: Weber and Rinne Test

A

sensori_N_EURAL lateralizes to _N_ORMAL ear and _N_ORMAL Rinne

  • Weber: Lateralizes to NORMAL ear. Thus, if lateralizes right, SNHL on left.
  • Rinne: AC> BC (though patient will still have difficulty hearing own voice and deciphering words)

__________

Etiologies

  • INNER EAR
  • Most common: Presbyacusis
  • Chronic loud noise exposure
  • CNS lesions (ex. acoustic neuroma)
  • Labyrinthitis
  • Meniere syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sensorineural Hearing Loss: Etiologies

A

__________

Etiologies

  • INNER EAR
  • Most common: Presbyacusis
  • Chronic loud noise exposure
  • CNS lesions (ex. acoustic neuroma)
  • Labyrinthitis
  • Meniere syndrome

_______

sensori_N_EURAL lateralizes to _N_ORMAL ear and _N_ORMAL Rinne

  • Weber: Lateralizes to NORMAL ear. Thus, if lateralizes right, SNHL on left.
  • Rinne: AC> BC (though patient will still have difficulty hearing own voice and deciphering words)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Meniere’s Disease (Idiopathic Endolymphatic Hydrops):

Pathophysiology

A

Pathophysiology

  • Idiopathic distention of endolymphatic compartment of inner ear by excess fluid
  • This results in increased pressure within the inner ear

Clinical Manifestations

  1. Episodic peripheral vertigo lasting minutes to hours
  2. Horizontal nystagmus (sign of peripheral vertigo)
  3. Tinnitus
  4. Ear fullness
  5. fluctuating hearing loss (primarily low tone hearing loss)
  6. Nausea
  7. Vomiting

Diagnosis

  • Transtympanic electrocochleography most accurate (during active episode)
  • Loss of nystagmus with caloric testing
  • Audiometry (loss of low tones)

Management

Symptomatic

  • antiemetics
  • antihistamines (Meclizine, Prochlorperazine)
  • Benzodiazepines (diazepam)
  • Anticholinergics (Scopolamine)
  • Decompression if refractory to meds or severe (ex. Typanostomy tube or Labyrinthectomy)

Preventative

  • Diuretics (hydrochlorothiazide): reduce endolymphatic pressure
  • Avoid: salt, caffeine, chocolate, ETOH (these increase endolymphatic pressure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Meniere’s Disease (Idiopathic Endolymphatic Hydrops):

Clinical Manifestations (7)

A

Clinical Manifestations

  1. Episodic peripheral vertigo lasting minutes to hours
  2. Horizontal nystagmus (sign of peripheral vertigo)
  3. Tinnitus
  4. Ear fullness
  5. fluctuating hearing loss (primarily low tone hearing loss)
  6. Nausea
  7. Vomiting

Diagnosis

  • Transtympanic electrocochleography most accurate (during active episode)
  • Loss of nystagmus with caloric testing
  • Audiometry (loss of low tones)

Management

Symptomatic

  • antiemetics
  • antihistamines (Meclizine, Prochlorperazine)
  • Benzodiazepines (diazepam)
  • Anticholinergics (Scopolamine)
  • Decompression if refractory to meds or severe (ex. Typanostomy tube or Labyrinthectomy)

Preventative

  • Diuretics (hydrochlorothiazide): reduce endolymphatic pressure
  • Avoid: salt, caffeine, chocolate, ETOH (these increase endolymphatic pressure)

Pathophysiology

  • Idiopathic distention of endolymphatic compartment of inner ear by excess fluid
  • This results in increased pressure within the inner ear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Meniere’s Disease (Idiopathic Endolymphatic Hydrops):

Diagnosis

A

Diagnosis

  • Transtympanic electrocochleography most accurate (during active episode)
  • Loss of nystagmus with caloric testing
  • Audiometry (loss of low tones)

Management

Symptomatic

  • antiemetics
  • antihistamines (Meclizine, Prochlorperazine)
  • Benzodiazepines (diazepam)
  • Anticholinergics (Scopolamine)
  • Decompression if refractory to meds or severe (ex. Typanostomy tube or Labyrinthectomy)

Preventative

  • Diuretics (hydrochlorothiazide): reduce endolymphatic pressure
  • Avoid: salt, caffeine, chocolate, ETOH (these increase endolymphatic pressure)

Pathophysiology

  • Idiopathic distention of endolymphatic compartment of inner ear by excess fluid
  • This results in increased pressure within the inner ear

Clinical Manifestations

  1. Episodic peripheral vertigo lasting minutes to hours
  2. Horizontal nystagmus (sign of peripheral vertigo)
  3. Tinnitus
  4. Ear fullness
  5. fluctuating hearing loss (primarily low tone hearing loss)
  6. Nausea
  7. Vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Meniere’s Disease (Idiopathic Endolymphatic Hydrops):

Management (Symptomatic and Preventative)

A

Management

Symptomatic

  • antiemetics
  • antihistamines (Meclizine, Prochlorperazine)
  • Benzodiazepines (diazepam)
  • Anticholinergics (Scopolamine)
  • Decompression if refractory to meds or severe (ex. Typanostomy tube or Labyrinthectomy)

Preventative

  • Diuretics (hydrochlorothiazide): reduce endolymphatic pressure
  • Avoid: salt, caffeine, chocolate, ETOH (these increase endolymphatic pressure)

Pathophysiology

  • Idiopathic distention of endolymphatic compartment of inner ear by excess fluid
  • This results in increased pressure within the inner ear

Clinical Manifestations

  1. Episodic peripheral vertigo lasting minutes to hours
  2. Horizontal nystagmus (sign of peripheral vertigo)
  3. Tinnitus
  4. Ear fullness
  5. fluctuating hearing loss (primarily low tone hearing loss)
  6. Nausea
  7. Vomiting

Diagnosis

  • Transtympanic electrocochleography most accurate (during active episode)
  • Loss of nystagmus with caloric testing
  • Audiometry (loss of low tones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acoustic (Vestibular) CN VIII Neuroma/Vestibular Schwannoma:

Pathophysiology

A

Pathophysiology

Cranial nerve VIII/8 Schwannoma-benign tumor of Schwann cells, which produce myelin sheath

Clinical Manifestation

**Unilateral SNHL is an acoustic neuroma until proven otherwise**

  1. Unilateral SNHL
  2. Tinnitus
  3. Headache
  4. Facial Numbness
  5. Continuous disequilibrium/vertigo (unsteadiness while walking)

Diagnosis

  • CT scan. Usually unilateral.
  • If bilateraly, suspect neurofribromatosis type II

Management

  • Surgery
  • Focused radiation therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acoustic (Vestibular) CN VIII Neuroma/Vestibular Schwannoma:

Clinical manifestation

A

Clinical Manifestation

**Unilateral SNHL is an acoustic neuroma until proven otherwise**

  1. Unilateral SNHL
  2. Tinnitus
  3. Headache
  4. Facial Numbness
  5. Continuous disequilibrium/vertigo (unsteadiness while walking)

Diagnosis

  • CT scan. Usually unilateral.
  • If bilateraly, suspect neurofribromatosis type II

Management

  • Surgery
  • Focused radiation therapy

Pathophysiology

Cranial nerve VIII/8 Schwannoma-benign tumor of Schwann cells, which produce myelin sheath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acoustic (Vestibular) CN VIII Neuroma/Vestibular Schwannoma:

Diagnosis

A

Diagnosis

  • CT scan. Usually unilateral.
  • If bilateraly, suspect neurofribromatosis type II

Management

  • Surgery
  • Focused radiation therapy

Pathophysiology

Cranial nerve VIII/8 Schwannoma-benign tumor of Schwann cells, which produce myelin sheath

Clinical Manifestation

**Unilateral SNHL is an acoustic neuroma until proven otherwise**

  1. Unilateral SNHL
  2. Tinnitus
  3. Headache
  4. Facial Numbness
  5. Continuous disequilibrium/vertigo (unsteadiness while walking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acoustic (Vestibular) CN VIII Neuroma/Vestibular Schwannoma:

Management

A

Management

  • Surgery
  • Focused radiation therapy

Pathophysiology

Cranial nerve VIII/8 Schwannoma-benign tumor of Schwann cells, which produce myelin sheath

Clinical Manifestation

**Unilateral SNHL is an acoustic neuroma until proven otherwise**

  1. Unilateral SNHL
  2. Tinnitus
  3. Headache
  4. Facial Numbness
  5. Continuous disequilibrium/vertigo (unsteadiness while walking)

Diagnosis

  • CT scan. Usually unilateral.
  • If bilateraly, suspect neurofribromatosis type II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

**Unilateral SNHL is an __________ until proven otherwise**

A

Acoustic (Vestibular) CN VIII Neuroma/Vestibular Schwannoma

Pathophysiology

Cranial nerve VIII/8 Schwannoma-benign tumor of Schwann cells, which produce myelin sheath

Clinical Manifestation

**Unilateral SNHL is an acoustic neuroma until proven otherwise**

  1. Unilateral SNHL
  2. Tinnitus
  3. Headache
  4. Facial Numbness
  5. Continuous disequilibrium/vertigo (unsteadiness while walking)

Diagnosis

  • CT scan. Usually unilateral.
  • If bilateraly, suspect neurofribromatosis type II

Management

  • Surgery
  • Focused radiation therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Barotrauma:

Pathophysiology

A

Pathophysiology

  • Rapid pressure change leads to the inability of the Eustachian Tube to equalize pressure
  • Symptoms similar to Eustachian Tube Dysfunction
  • Ex: taking a flight on an airplane, scuba diver, or patients on mechanical ventilation

Clinical Manifestations

  1. Auricular pain and fullness
  2. Hearing loss that persists after the etiologic event
  3. May have bloody discharge if traumatic
  4. Tympanic Membrane: +/- rupture or petechiae

Management

  • Autoinsufflation (swallowing, yawning)
  • Decongestants or antihistamines (reduce eustachian tube edema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Barotrauma:

Clinical Manifestations (4)

A

Clinical Manifestations

  1. Auricular pain and fullness
  2. Hearing loss that persists after the etiologic event
  3. May have bloody discharge if traumatic
  4. Tympanic Membrane: +/- rupture or petechiae

Management

  • Autoinsufflation (swallowing, yawning)
  • Decongestants or antihistamines (reduce eustachian tube edema)

Pathophysiology

  • Rapid pressure change leads to the inability of the Eustachian Tube to equalize pressure
  • Symptoms similar to Eustachian Tube Dysfunction
  • Ex: taking a flight on an airplane, scuba diver, or patients on mechanical ventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Barotrauma:

Management

A

Management

  • Autoinsufflation (swallowing, yawning)
  • Decongestants or antihistamines (reduce eustachian tube edema)

Pathophysiology

  • Rapid pressure change leads to the inability of the Eustachian Tube to equalize pressure
  • Symptoms similar to Eustachian Tube Dysfunction
  • Ex: taking a flight on an airplane, scuba diver, or patients on mechanical ventilation

Clinical Manifestations

  1. Auricular pain and fullness
  2. Hearing loss that persists after the etiologic event
  3. May have bloody discharge if traumatic
  4. Tympanic Membrane: +/- rupture or petechiae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Patient is experiencing a “false sense of motion” or “exaggerated sense of motion”. What is the terminology for this?

A

Vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vertigo

Location of problem: Peripheral vertigo

A

Peripheral Vertigo

Location of problem

  • Labyrinth or vestibular nerve (which is part of CNVIII/8)

Etiologies

  1. ​Benign Positional Vertigo (BPV) (most common)
  2. Meniere
  3. Vestibular Neuritis
  4. Labyrinthitis
  5. Cholesteatoma

Clinical

  1. HORIZONTAL nystagmus (usually beats away from affected side)
  2. Fatigable
  3. Sudden onset of tinnitus and hearing loss usually associated with peripheral compared to central causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Vertigo

Etiologies: Peripheral vertigo

A

Peripheral Vertigo

Etiologies

  1. ​Benign Positional Vertigo (BPV) (most common)
  2. Meniere
  3. Vestibular Neuritis
  4. Labyrinthitis
  5. Cholesteatoma

Clinical

  1. HORIZONTAL nystagmus (usually beats away from affected side)
  2. Fatigable
  3. Sudden onset of tinnitus and hearing loss usually associated with peripheral compared to central causes

Location of problem

  • Labyrinth or vestibular nerve (which is part of CNVIII/8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Vertigo

Clinical Presentation: Peripheral vertigo

A

Peripheral Vertigo

Clinical

  1. HORIZONTAL nystagmus (usually beats away from affected side)
  2. Fatigable
  3. Sudden onset of tinnitus and hearing loss usually associated with peripheral compared to central causes

Location of problem

  • Labyrinth or vestibular nerve (which is part of CNVIII/8)

Etiologies

  1. ​Benign Positional Vertigo (BPV) (most common)
  2. Meniere
  3. Vestibular Neuritis
  4. Labyrinthitis
  5. Cholesteatoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Vertigo

  1. Episodic vertigo
  2. No hearing loss
A

Peripheral Vertigo

  • ​Benign Positional Vertigo (BPV) (most common)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Vertigo

  1. Episodic vertigo
  2. Positive for hearing loss
A

Peripheral Vertigo

  • Meniere
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vertigo

  1. Continuous vertigo
  2. Positive for hearing loss
A

Peripheral Vertigo

  • Labyrinthitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Vertigo

  1. Continuous vertigo
  2. No hearing loss
A

Peripheral Vertigo

  • Vestibular Neuritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Vertigo

Pathophysiology of nausea and vomiting

A

Nausea and vomiting are caused by sensory conflict mediated by the neurotransmitters GABA, acetylcholine, histamine, dopamine, and serotonin. Antiemetics work primarily by these transmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Vertigo

Identify which type of vertigo:

  • HORIZONTAL nystagmus
  • Fatigable
A

Peripheral Vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Vertigo

Identify which type of vertigo:

  • VERTICAL nystagmus
  • NONFatigable (continuous)
A

Central Vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Vertigo

Central Vertigo: Location of problem

A

Central Vertigo

Location of problem

Brainstem or cerebellar

Etiologies

  1. Cerebellopontine tumors
  2. Migraine
  3. Cerebral vascular disease
  4. Multiple sclerosis
  5. Vestibular neuroma

Clinical

  1. VERTICAL nystagmus
  2. NONfatigable (continuous)
  3. Gait problems more severe
  4. Gradual onset
  5. Positive CNS signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Vertigo

Central Vertigo: possible etiologies (5)

A

Central Vertigo

Etiologies

  1. Cerebellopontine tumors
  2. Migraine
  3. Cerebral vascular disease
  4. Multiple sclerosis
  5. Vestibular neuroma

Clinical

  1. VERTICAL nystagmus
  2. NONfatigable (continuous)
  3. Gait problems more severe
  4. Gradual onset
  5. Positive CNS signs

Location of problem

Brainstem or cerebellar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Vertigo

Central Vertigo: clinical manifestations (5)

A

Central Vertigo

Clinical

  1. VERTICAL nystagmus
  2. NONfatigable (continuous)
  3. Gait problems more severe
  4. Gradual onset
  5. Positive CNS signs

Location of problem

Brainstem or cerebellar

Etiologies

  1. Cerebellopontine tumors
  2. Migraine
  3. Cerebral vascular disease
  4. Multiple sclerosis
  5. Vestibular neuroma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Vertigo: What is your first line for managing Nausea/Vomiting in patients with vertigo? Other treatments?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the most common cause of vertigo?

A

Benign Positional Vertigo (BPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Benign Paroxysmal Positional Vertigo (BPV or BPPV)

Pathophysiology

A

Pathophysiology

  • Caused by displaced otoliths (calcium carbonate particles)
  • Normally, otoliths are attached to the hair cells inside the saccule and utricule (attached to the 3 semicircular canals)
  • Head movements cause displaced otolith movement, which leads to vertigo

Clinical manifestations

  1. ​Sudden, episodic peripheral vertigo (provoked with changes of head positioning)
    • Vertigo usually lasts 10-60 seconds
  2. Positive Dix-Hallpike Test/Nylan Barany
    • Patient placed in supine position with head 30 degrees lower than body
    • Head quickly turned 90 degrees to one side
    • Result: Delayed fatigable horizontal nystagmus
    • IF NYSTAGMUS IS PERSISTANT OR NON-FATIGABLE, ASSESS FOR CENTRAL CAUSE OF VERTIGO INSTEAD.

Management

  1. Epley maneuver
    • Canalith repositioning mainstay of treatment
    • Usually resolves with time as the otoliths naturally dissolve and the vertigo episodic brief
  2. Medications usually not needed. But, if medicate:
    • antihistamines,
    • anticholinergics,
    • benzodiazepines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Benign Paroxysmal Positional Vertigo (BPV or BPPV)

Clinical Manifestations

A

Clinical manifestations

  1. ​Sudden, episodic peripheral vertigo (provoked with changes of head positioning)
    • Vertigo usually lasts 10-60 seconds
  2. Positive Dix-Hallpike Test/Nylan Barany
    • Patient placed in supine position with head 30 degrees lower than body
    • Head quickly turned 90 degrees to one side
    • Result: Delayed fatigable horizontal nystagmus
    • IF NYSTAGMUS IS PERSISTANT OR NON-FATIGABLE, ASSESS FOR CENTRAL CAUSE OF VERTIGO INSTEAD.

Management

  1. Epley maneuver
    • Canalith repositioning mainstay of treatment
    • Usually resolves with time as the otoliths naturally dissolve and the vertigo episodic brief
  2. Medications usually not needed. But, if medicate:
    • antihistamines,
    • anticholinergics,
    • benzodiazepines

Pathophysiology

  • Caused by displaced otoliths (calcium carbonate particles)
  • Normally, otoliths are attached to the hair cells inside the saccule and utricule (attached to the 3 semicircular canals)
  • Head movements cause displaced otolith movement, which leads to vertigo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Benign Paroxysmal Positional Vertigo (BPV or BPPV)

Management

A

Management

  1. Epley maneuver
    • Canalith repositioning mainstay of treatment
    • Usually resolves with time as the otoliths naturally dissolve and the vertigo episodic brief
  2. Medications usually not needed. But, if medicate:
    • antihistamines,
    • anticholinergics,
    • benzodiazepines

Pathophysiology

  • Caused by displaced otoliths (calcium carbonate particles)
  • Normally, otoliths are attached to the hair cells inside the saccule and utricule (attached to the 3 semicircular canals)
  • Head movements cause displaced otolith movement, which leads to vertigo

Clinical manifestations

  1. ​Sudden, episodic peripheral vertigo (provoked with changes of head positioning)
    • Vertigo usually lasts 10-60 seconds
  2. Positive Dix-Hallpike Test/Nylan Barany
    • Patient placed in supine position with head 30 degrees lower than body
    • Head quickly turned 90 degrees to one side
    • Result: Delayed fatigable horizontal nystagmus
    • IF NYSTAGMUS IS PERSISTANT OR NON-FATIGABLE, ASSESS FOR CENTRAL CAUSE OF VERTIGO INSTEAD.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Anatomy and functions of the Labyrinth

A

Labyrinth: The bony and membranous part of the inner ear. Consists of 2 components:

  1. Cochlea: responsible for hearing (converts wave impulses from middle ear into auditory nerve impulses)
  2. vestibular system: 3 semicircular canals originating in the vestibule responsible for balance.
35
Q

Vestibular Neuritis+ Labyrinthitis

Pathophysiology

A

Pathophysiology

  • Vestibular Neuritis: Inflammation fo the vestibular portion of CN 8
  • Labyrinthitis: vestibular neuritis AND hearing loss/tinnitus (from cochlear involvement)

Clinical manifestations

Vestibular symptoms

  1. peripheral vertigo (usually continuos)
    • nystagmus HORIZONTAL and rotary (away from the affected side)
  2. dizziness
  3. nausea/vomiting
  4. gait disturbances

Cochlear symptoms

  1. hearing loss (usually resolve in weeks)

Management

  • 1st line: corticosteroids
  • If symptomatic: antihistamines (Meclizine)
  • If symptomatic: benzodiazepines
36
Q

Vestibular Neuritis+ Labyrinthitis

Clinical manifestations (vestibular (4) and cochlear (1))

A

Clinical manifestations

Vestibular symptoms

  1. peripheral vertigo (usually continuos)
    • nystagmus HORIZONTAL and rotary (away from the affected side)
  2. dizziness
  3. nausea/vomiting
  4. gait disturbances

Cochlear symptoms

  1. hearing loss (usually resolve in weeks)

Management

  • 1st line: corticosteroids
  • If symptomatic: antihistamines (Meclizine)
  • If symptomatic: benzodiazepines

Pathophysiology

  • Vestibular Neuritis: Inflammation fo the vestibular portion of CN 8
  • Labyrinthitis: vestibular neuritis AND hearing loss/tinnitus (from cochlear involvement)
37
Q

Vestibular Neuritis+ Labyrinthitis

Management

A

Management

  • 1st line: corticosteroids
  • If symptomatic: antihistamines (Meclizine)
  • If symptomatic: benzodiazepines

Pathophysiology

  • Vestibular Neuritis: Inflammation fo the vestibular portion of CN 8
  • Labyrinthitis: vestibular neuritis AND hearing loss/tinnitus (from cochlear involvement)

Clinical manifestations

Vestibular symptoms

  1. peripheral vertigo (usually continuos)
    • nystagmus HORIZONTAL and rotary (away from the affected side)
  2. dizziness
  3. nausea/vomiting
  4. gait disturbances

Cochlear symptoms

  1. hearing loss (usually resolve in weeks)
38
Q

Vestibular Neuritis+ Labyrinthitis

Describe the nystagmus expected

A

nystagmus HORIZONTAL and rotary (away from the affected side)

_________________

Pathophysiology

  • Vestibular Neuritis: Inflammation fo the vestibular portion of CN 8
  • Labyrinthitis: vestibular neuritis AND hearing loss/tinnitus (from cochlear involvement)

Clinical manifestations

Vestibular symptoms

  1. peripheral vertigo (usually continuos)
    • nystagmus HORIZONTAL and rotary (away from the affected side)
  2. dizziness
  3. nausea/vomiting
  4. gait disturbances

Cochlear symptoms

  1. hearing loss (usually resolve in weeks)

Management

  • 1st line: corticosteroids
  • If symptomatic: antihistamines (Meclizine)
  • If symptomatic: benzodiazepines
39
Q

Acute Otitis Media

Primary differences between Acute Otitis Media and Otitis Media with Effusion

A

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan
40
Q

Acute Otitis Media

Pathophysiology

A

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan
41
Q

Acute Otitis Media

Primary organisms (4)

A

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora
42
Q

Acute Otitis Media

Most common organism responsible

A

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora
43
Q

Acute Otitis Media

Risk factors

A

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes
44
Q

Acute Otitis Media

Peak age

A

Peak age 6-18 months.

________________

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes
45
Q

Acute Otitis Media

Often preceded by what?

A

Most commonly preceded by a viral URI

________________

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan
46
Q

Acute Otitis Media

Clinical manifestations

A

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed
47
Q

Acute Otitis Media

Expected clinical manifestation if TM perforation? How long to heal?

A

If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

_____________

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed
48
Q

Acute Otitis Media

Expected result on pneumatic otoscopy

A

Decreased tympanic membrane mobility on pneumatic otoscopy

_____________

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)
49
Q

Acute Otitis Media

physical exam findings: what organism should you suspect if bullae are present?

A

If bullae on TM, suspect Mycoplasma pneumoniae

_____________

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)
50
Q

Acute Otitis Media

physical exam findings

A

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)
51
Q

Acute Otitis Media

management

A

Management

  1. Antibiotics:
    • 1st: Amoxicillin treatment. Cefixime in children.
    • 2nd: Amoxicillin/clavulanic acid (augmentin) or cefaclor.
    • If PCN allergic: Erythromycin-sulfisoxazole, azithromycin, trimethoprim/sulfamethoxazole.
  2. Severe/recurrent cases:
    • Myringotomy (surgical drainage)
    • Tympanostomy if recurrent or persistent
  3. Otitis Media with effusion: observation in most cases
    • In children with recurrent otitis media: iron deficiency anemia work up and CT scan

Acute Otitis Media v. Otitis Media with effusion

  • Acute: rapid onset and signs/symptoms of inflammation
  • OM with effusion: asymptomatic/no inflammation

Pathophysiology

  • Infection of the middle ear, temporal bone, and mastoid air cells
  • Most commonly preceded by a viral URI
  • URI causes eustachian tube edema, resulting in negative pressure and transudation of fluid and mucus in middle ear
  • Secondary: colonization by bacteria and flora

Organisms

  1. S. pneumo (most common)
  2. H. influenza
  3. Moraxella catarrhalis
  4. Strep pyogenes

Risk Factors

  1. Eustachian tube dysfunction (ETD)
  2. Young (Eustachian tube is wider, shorter, and more horizontal). Peak age 6-18 months.
  3. Day care
  4. Pacifier/bottle use
  5. Parental smoking
  6. Not being breastfed

Clinical Manifestations

  1. Fever
  2. otalgia (ear pain)
  3. Ear tugging in infants
  4. conductive hearing loss
  5. stuffiness
  6. If TM perforation: rapid relief of pain and otorrhea (will heal in 1-2 days)

Physical Exam

  1. Bulging, erythematous tympanic membrane with effusion
    • Loss of landmarks
    • Decreased tympanic membrane mobility on pneumatic otoscopy
  2. If bullae on TM, suspect Mycoplasma pneumoniae
52
Q

Chronic Otitis Media

Etiologies

A

Etiologies

Complication of:

  1. acute otitis media,
  2. trauma, or
  3. due to cholesteatoma

Organisms

  1. Pseudomonas
  2. S. aureus
  3. Gram negative rods (proteus)
  4. anaerobes
  5. Mycoplasma

Clinical manifestations

  1. Perforated TM
  2. Persistent or recurrent purulent otorrhea
  3. May/may not have pain
  4. May have varying degrees of conductive hearing loss
  5. May/may not have cholesteatoma

Management

  1. Topical antibiotics (first line treatment) ex. Oflaxacin or Ciprofloxacin
  2. Surgical
    • tympanic membrane repair/reconstruction
    • If severe, mastoidectomy
  3. Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture
53
Q

Chronic Otitis Media

Organisms

A

Organisms

  1. Pseudomonas
  2. S. aureus
  3. Gram negative rods (proteus)
  4. anaerobes
  5. Mycoplasma

Clinical manifestations

  1. Perforated TM
  2. Persistent or recurrent purulent otorrhea
  3. May/may not have pain
  4. May have varying degrees of conductive hearing loss
  5. May/may not have cholesteatoma

Management

  1. Topical antibiotics (first line treatment) ex. Oflaxacin or Ciprofloxacin
  2. Surgical
    • tympanic membrane repair/reconstruction
    • If severe, mastoidectomy
  3. Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Etiologies

Complication of:

  1. acute otitis media,
  2. trauma, or
  3. due to cholesteatoma
54
Q

Chronic Otitis Media

clinical manifestations

A

Clinical manifestations

  1. Perforated TM
  2. Persistent or recurrent purulent otorrhea
  3. May/may not have pain
  4. May have varying degrees of conductive hearing loss
  5. May/may not have cholesteatoma

Management

  1. Topical antibiotics (first line treatment) ex. Oflaxacin or Ciprofloxacin
  2. Surgical
    • tympanic membrane repair/reconstruction
    • If severe, mastoidectomy
  3. Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Etiologies

Complication of:

  1. acute otitis media,
  2. trauma, or
  3. due to cholesteatoma

Organisms

  1. Pseudomonas
  2. S. aureus
  3. Gram negative rods (proteus)
  4. anaerobes
  5. Mycoplasma
55
Q

Chronic Otitis Media

Management

A

Management

  1. Topical antibiotics (first line treatment) ex. Oflaxacin or Ciprofloxacin
  2. Surgical
    • tympanic membrane repair/reconstruction
    • If severe, mastoidectomy
  3. Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Etiologies

Complication of:

  1. acute otitis media,
  2. trauma, or
  3. due to cholesteatoma

Organisms

  1. Pseudomonas
  2. S. aureus
  3. Gram negative rods (proteus)
  4. anaerobes
  5. Mycoplasma

Clinical manifestations

  1. Perforated TM
  2. Persistent or recurrent purulent otorrhea
  3. May/may not have pain
  4. May have varying degrees of conductive hearing loss
  5. May/may not have cholesteatoma
56
Q

Chronic Otitis Media

Management: If TM rupture, what do you avoid?

A

Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

________

Management

  1. Topical antibiotics (first line treatment) ex. Oflaxacin or Ciprofloxacin
  2. Surgical
    • tympanic membrane repair/reconstruction
    • If severe, mastoidectomy
  3. Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Etiologies

Complication of:

  1. acute otitis media,
  2. trauma, or
  3. due to cholesteatoma

Organisms

  1. Pseudomonas
  2. S. aureus
  3. Gram negative rods (proteus)
  4. anaerobes
  5. Mycoplasma

Clinical manifestations

  1. Perforated TM
  2. Persistent or recurrent purulent otorrhea
  3. May/may not have pain
  4. May have varying degrees of conductive hearing loss
  5. May/may not have cholesteatoma
57
Q

Mastoiditis

Etiology/pathophysiology

A

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy
58
Q

Mastoiditis

Clinical manifestation

A

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected
59
Q

Mastoiditis

At what time of day do you expect the deep ear pain to be worse?

A

Deep ear pain (usually worse at night)

_________

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected
60
Q

Mastoiditis

What might develop in relation to the mastoid tenderness?

A

Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

_________

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected
61
Q

Mastoiditis

Complications

A

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)
62
Q

Mastoiditis

Diagnosis

A

Diagnosis

  1. CT scan is 1st line diagnostic test

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess
63
Q

Mastoiditis

Management

A

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Diagnosis

  1. CT scan is 1st line diagnostic test
64
Q

Mastoiditis

Complications: which cranial nerve is at risk for paralysis?

A

CN VII/7 paralysis

______________

Complications

  1. hearing loss
  2. labyrinthitis
  3. vertigo
  4. CN VII paralysis
  5. brain abscess

Management

First line:

  • IV antibiotics (same as acute otitis media antibiotics) AND middle ear/mastoid drainage via myringotomy with or without tympanostomy tube placement.
  • Tympanocentesis can be performed to obtain a middle ear culture

If refractory or complicated:

  • mastoidectomy

Etiology/Pathophysiology

  • Inflammation of the mastoid air cells of the temporal bone
  • Usually a complication of prolonged or inadequately treated otitis media
  • All patients with acute otitis media have some degree of mastoiditis because the mastoid and middle ear are connected

Clinical manifestations

  1. Deep ear pain (usually worse at night)
  2. Fever
  3. Mastoid tenderness (may develop cutaneous abscess) (fluctuance)

Diagnosis

  1. CT scan is 1st line diagnostic test
65
Q

Otosclerosis

pathophysiology

A

Pathophysiology

  • Abnormal bony overgrowth of the stapes bone
  • This leads to conductive hearing loss due to blocked conduction

Clinical manifestation

  1. slowly progressive conductive hearing loss
  2. tinnitus
  3. vertigo is uncommon

Management

  • stapedectomy with prosthesis
  • Hearing aid
  • Cochlear implantation if severe
66
Q

Otosclerosis

clinical manifestation

A

Clinical manifestation

  1. slowly progressive conductive hearing loss
  2. tinnitus
  3. vertigo is uncommon

Management

  • stapedectomy with prosthesis
  • Hearing aid
  • Cochlear implantation if severe

Pathophysiology

  • Abnormal bony overgrowth of the stapes bone
  • This leads to conductive hearing loss due to blocked conduction
67
Q

Otosclerosis

management

A

Management

  • stapedectomy with prosthesis
  • Hearing aid
  • Cochlear implantation if severe

Pathophysiology

  • Abnormal bony overgrowth of the stapes bone
  • This leads to conductive hearing loss due to blocked conduction

Clinical manifestation

  1. slowly progressive conductive hearing loss
  2. tinnitus
  3. vertigo is uncommon
68
Q

Cholesteatoma

pathophysiology

A

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles
69
Q

Cholesteatoma

Commonly due to what?

A

Commonly due to Eustachian Tube Dysfunction

_________________

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles
70
Q

Cholesteatoma

Describe the otorrhea discharge

A
  • painless
  • brown/yellow discharge with strong odor

_________________

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss
71
Q

Cholesteatoma

clinical manifestation

A

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss
72
Q

Cholesteatoma

diagnosis

A

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness
73
Q

Cholesteatoma

management

A

Management

  • surgical excision of the debris/cholesteatoma
  • reconstruction of the ossicles

Pathophysiology

  • Abnormal keratinized collection of desquamated squamous epithelium (mastoid bony erosion)
  • Commonly due to Eustachian Tube Dysfunction such that:
    • chronic negative pressure inverts part of the tympanic membrane
    • the granulation tissue erodes the ossicles over time,
    • resulting in conductive hearing loss

​Clinical Manifestation

  1. painless otorrhea (brown/yellow discharge with strong odor)
  2. May/may not have vertigo/dizziness

Diagnosis

  • Otoscope:
    • Granulation tissue (cellular debris)
    • May/man not have perforation of the tympanic membrane
  • Peripheral vertigo
  • Conductive hearing loss
    • weber lateralization to affected ear
    • rinne: BC>/equal to AC
74
Q

Eustachian Tube Dysfunction

Pathophysiology

A

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged
75
Q

Eustachian Tube Dysfunction

What type of pressure?

A
  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure

_​____________

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged
76
Q

Eustachian Tube Dysfunction

clinical manifestations

A

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis
77
Q

Eustachian Tube Dysfunction

diagnosis

A

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus
78
Q

Eustachian Tube Dysfunction

management

A

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media
79
Q

Eustachian Tube Dysfunction

complications

A

Complications

  1. Acute serous otitis media (non infectious fluid in middle ear)
  2. The above may become colonized by bacteria and result in infectious otitis media if prolonged

Pathophysiology

  • Eustachian tube swelling inhibits ET’s autoinsuffflation ability
  • This leads to negative pressure
  • Often follows viral URI or allergic rhinitis

Clinical manifestations

  1. Ear fullness
  2. popping of ears/underwater feeling
  3. intermittent sharp ear pain
  4. disequilibrium
  5. fluctuating CHL
  6. tinnitus

Diagnosis

  • Otoscopic findings usually normal
  • May, may not have fluid behind TM if acute serous otitis media

Management

  1. Decongestants (lowers ET edema): pseudoephedrine, phenylephrine, oxymetazoline nasal spray
  2. Autoinsufflation (swallowing, yawning, blowing against a slightly pitched nostril)
  3. Intranasal corticosteroids
80
Q

Tympanic membrane perforation

Most common causes

A

Most common cause

  • Occurs due to penetrating or noise trauma or otitis media
  • Most commonly occurs at pars tensa

Clinical manifestations

  • Acute ear pain
  • hearing loss
  • may, may not have bloody otorrhea
  • may, may not have tinnitus and vertigo

Diagnosis

  • Otoscope exam: perforated TM. May lead to cholesteatoma development
  • may, may not have CHL
    • Weber: lateralization to affected ear
    • Rinne: BC>/equal to AC

Management

  • Most perforated TM will heal spontaneously. Follow to ensure resolution. Surgical options available.
  • Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture
81
Q

Tympanic membrane perforation

clinical manifestation

A

Clinical manifestations

  • Acute ear pain
  • hearing loss
  • may, may not have bloody otorrhea
  • may, may not have tinnitus and vertigo

Diagnosis

  • Otoscope exam: perforated TM. May lead to cholesteatoma development
  • may, may not have CHL
    • Weber: lateralization to affected ear
    • Rinne: BC>/equal to AC

Management

  • Most perforated TM will heal spontaneously. Follow to ensure resolution. Surgical options available.
  • Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Most common cause

  • Occurs due to penetrating or noise trauma or otitis media
  • Most commonly occurs at pars tensa
82
Q

Tympanic membrane perforation

diagnosis

A

Diagnosis

  • Otoscope exam: perforated TM. May lead to cholesteatoma development
  • may, may not have CHL
    • Weber: lateralization to affected ear
    • Rinne: BC>/equal to AC

Management

  • Most perforated TM will heal spontaneously. Follow to ensure resolution. Surgical options available.
  • Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Most common cause

  • Occurs due to penetrating or noise trauma or otitis media
  • Most commonly occurs at pars tensa

Clinical manifestations

  • Acute ear pain
  • hearing loss
  • may, may not have bloody otorrhea
  • may, may not have tinnitus and vertigo
83
Q

Tympanic membrane perforation

management

A

Management

  • Most perforated TM will heal spontaneously. Follow to ensure resolution. Surgical options available.
  • Avoid water/moisture/topical aminoglycosides in the ear whenever there is a TM rupture

Most common cause

  • Occurs due to penetrating or noise trauma or otitis media
  • Most commonly occurs at pars tensa

Clinical manifestations

  • Acute ear pain
  • hearing loss
  • may, may not have bloody otorrhea
  • may, may not have tinnitus and vertigo

Diagnosis

  • Otoscope exam: perforated TM. May lead to cholesteatoma development
  • may, may not have CHL
    • Weber: lateralization to affected ear
    • Rinne: BC>/equal to AC

2017 EENT Clin Med Group (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions