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Otology & Neurotology > Temporal Bone Trauma and Barotrauma > Flashcards

Temporal Bone Trauma and Barotrauma Flashcards

1
Q

Name 3 types of barotrauma

A
  1. Alternobaric vertigo (sometimes called alternobaric trauma) - On Ascent
  2. Atmospheric inner ear barotrauma - On Descent
  3. Inner ear decompression sickness and isobaric gas counter diffusion sickness
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2
Q

What is Alternobaric Vertigo?
What is the mechanism of vertigo?
How is it relieved? 1
What are the symptoms - 4

A

Definition: An asymmetrical increase in middle ear pressure due to decreasing ambient pressure, most prominent in ascent while diving or flying, leading to vertigo
- ie. “Decrease atmospheric pressure, ascent”
- Reverse Squeeze

Possible mechanism of vertigo:
- Transmission of pressure from the middle ear to the inner ear occurs when changes in middle ear pressure occur
- This causes stapes to be pushed in and oval windows to vibrate –> affecfts endolymphatic flow –> alteration in the activity of the primary vestibular neurons - Leads to a pressure-induced vestibular

Relieved by: Equilibration of middle ear and ambient pressure

Symptoms:
- Vertigo
- Hearing loss
- Tinnitus
- Short duration (10-15 minutes)

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3
Q

Discuss Atmospheric Inner Ear Barotrauma.
When does it typically occur?
What are the 2 pathophysiology mechanisms?
What are the symptoms?
What are 3 main treatments?
What is absolutely contraindicated?

A

Definition: Occurs due to significant sudden pressure changes placed on the inner ear
- e.g. sudden increase in atmospheric pressure, descent (decrease inner ear pressure)

Pathophysiology of inner ear barotrauma:
- Seen either with implosion (RW/OW displaced into labyrinth); OR
- Explosion (high intracranial pressure transmitted to the inner ear or middle ear pressure drops suddenly, and RW/OW is sucked out)

Symptoms:
- Tinnitis most common
- Hearing loss
- Vertigo occurs less frequently

Prognosis:
- Often permanent or long lasting

Treatment:
- Hyperbaric oxygen is CONTRAINDICATED!! (worsens the barotrauma) –> Very important to differentiate from inner ear decompression sickness
- Conservative: Bed rest, head elevation, avoidance of activities that elevate CSF pressure
- Surgical exploration for HL progression or failure of symptom resolution in 3-5 days
- Long term: Divers who fail to recover 100% should not return to diving

Examples:
- Sudden descent of a diver

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4
Q

What are the proposed mechanisms for implosive and explosive damage to the inner ear in Atmospheric inner ear Barotrauma?

A
  • Middle ear pressure becomes negative relative to intralabyrinthine fluid pressure in the presence of inadequate middle ear clearing during descent.
  • A diver tries to clear the ear (modified valsalva), leading to either
  1. THE EXPLOSIVE MECHANISM
    - Fail to equilibrate the middle ear pressure
    - However, intralabyrinthine fluid pressure via the cochlear aqueduct or the IAC still remains relatively higher
    - This leads to an increase in the differential between the perilymph and the middle ear cavity
    - This causes rupture outward of the round or oval window –> perilymph fistula –> SNHL and vertigo
  2. THE IMPLOSIVE MECHANISM
    - With sudden, forceful, modified valsalva, a rapid increase in middle ear pressure occurs, causing a relative “push” of the RW/OW –> leads to a rupture of the RW or OW and thus a perilymph fisult
    - Another improsive injury theory: Negative middle ear pressure causes inward displacement of the ossicles –> subluxation of the stapes footplate –> oval window fistula
    - Implosive mechanism considered much less frequent than the explosive injury
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5
Q

What is the physics gas law that is responsible for atmospheric inner ear barotrauma? At what level is guaranteed rupture?

A

Boyle’s Law: P1xV1 = P2xV2

Shallow dives and low altitude flights have the highest risk for barotrauma.
- Greatest pressure difference occurs in the first 10m of the dive

TM may rupture @ 260mmHg (35kP)

Guaranteed rupture = 750mmHg

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6
Q

Discuss inner ear decompression sickness and isobaric gas counter diffusion sickness

A
  • Formation of gas bubbles in the body occurs due to RAPID reduction in atmospheric pressure (ascent) or too rapid an exchange of inspired gas mixtures under isobaric conditions (ie. deep sea diving)

Key: Occurs during RAPID ascent

Symptoms:
1. Vertigo (most common - 50% sole complaine in IEDS)
2. SNHL
3. Tinnitus
4. Other: fatigue, pain in muscles/joints, paresthesias, weakness, difficulty breathing, chest pain

TREATMENT:
1. Rapid recompression (hyperbaric oxygen)

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7
Q

What should you ask a diver on history to help differentiate between atmospheric inner ear barotrauma and inner ear decompression sickness?

A

History:
- The dive profile and characteristics such as: decompression time required, omitted decompression, rapid ascent or descent, and gas mixtures used
- Onset of symptoms during descent or ascent, or shortly after decompression
- Associated symptoms such as other decompression sickness symptoms
- Difficulty in clearing ears, pre-existing otologic complaints, nasal or sinus complaints

ATMOSPHERIC INNER EAR BAROTRAUMA:
1. Shallow dives
2. On descent
3. Associated with equalization problems
4. Forceful valsalva
5. No non-otologic neurologic findings

INNER EAR DECOMPRESSION SICKNESS:
1. Deep and prolonged dives that may have omitted appropriate decompression steps
2. On ascent or shortly after ascent
3. Not associated with pressure equalization problems
4. Extraotologic neurologic findings

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8
Q

List the 5 grades of middle ear barotrauma (Edmonds Grading)

A

EDMONDS GRADING:

  • Grade 0: Symptoms without signs
  • Grade 1: Diffuse redness and retraction
  • Grade 2: As above, plus slight hemorrhage within the tympanic membrane
  • Grade 3: As above, plus gross hemorrhage within the tympanic membrane
  • Grade 4: Dark and slightly bulging TM with free blood in the middle ear and possible air/fluid level
  • Grade 5: Above plus TM perforation
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9
Q

Describe the Teed scale to evaluate middle ear barotrauma

A

0 - No visible damage, normal ear
1 - Congestion around the umbo, occurs with a pressure differential of 2 pounds per square inch (PSI)
2 - Congestion of entire TM, occurs with a pressure differential of 2-3 PSI
3 - Hemorrhage into the middle ear
4 - Extensive middle ear hemorrhage with blood bubbles visible behind TM, TM may rupture
5 - Entire middle ear filled with dark (deoxygenated) blood

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10
Q

What is the management of an uncomplicated tympanic membrane perforation after barotrauma?

A
  1. Observation
  2. Minor patch (paper patch)
  3. Myringoplasty/tympanoplasty
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11
Q

What area of the TM is most susceptible to barotrauma?

A

Pars Tensa

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12
Q

Describe how to classify temporal bone fractures?

A

NEW TERMINOLOGY:
1. Otic capsule involving (40% facial nerve injury)
2. Otic capsule sparing (most common - 90%) - 20% ossicular chain disruption, < 10% facial nerve injury

Older terminology:
- Transverse and longitudinal fractures

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13
Q

Discuss longitudinal temporal bone fractures, regarding:
1. Frequency
2. Cause
3. Clinical presentation - 4
4. Course of fracture through the temporal bone

A

Longitudinal = Saggital plane

Frequency ~80%

CAUSE:
- Due to lateral impacts, often with tearing of TM and hemotympanum

CLINICAL PRESENTATION:
1. Conductive hearing loss
2. Vestibular involvement mild (concussive)
3. CSF leak ~20%
4. Facial nerve paralysis of delayed onset ~20% if fallopian canal damaged (will usually be in tympanic segment)

COURSE OF FRACTURE THROUGH TB: Petrosquamous suture, Through EAC 7 tympanic ring, Fractures tegmen, Avoids otic capsule, Runs through foramen lacerum, Foramen ovale, and/or eustachian tube

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14
Q

Regarding transverse temporal bone fractures, discuss:
1. Frequency
2. Cause
3. Clinical presentation
4. Course of fracture through the temporal bone

A

Transverse = Axial (posterior to anterior)

Frequency ~ 20%

CAUSE:
1. Due to occipitomastoid trauma, usually of high energy

CLINICAL PRESENTATION:
1. Present with significant SNHL and vestibular dysfunction
2. ~50% CNVII paralysis of immediate onset

COURSE OF FRACTURE THROUGH TB: Through jugular foramen & foramen magnum, courses through otic capsule through vestibule or medial IAC, then through foramen spinosum & lacerum

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15
Q

Discuss the broad classification of temporal bone trauma

A
  1. Penetrating
  2. Blunt
  3. Blast
  4. Barotraumas
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16
Q

List 5 indications to obtain a CT of the temporal bones in a trauma cause

A
  1. Facial paralysis
  2. CSF leak
  3. Disruption of superior EAC (MCF injury)
  4. Suspected vascular injury
  5. If planning surgery for otologic complication
17
Q

List 7 different types of otologic complications that can occur with temporal bone trauma?

A
  1. SNHL
  2. CHL
  3. CSF leak
  4. Facial nerve injury
  5. Meningitis
  6. Transient or prolonged vertigo
  7. Hemotympanum
18
Q

If a patient has SNHL after head trauma however CT TB is normal, what are the suspected etiologies? 3

A
  1. Labyrinthine concussion - self-limiting acute vertigo, recoverable SNHL and tinnitus, possibly due to hemorrhage into labyrinth
  2. Shearing of cochlear nerve fibers
  3. Traumatic hydrops - fistula, ELS (endolymphatic sac) blockage, increased ICP from bleeding
19
Q

What are the most common ossicular injuries in temporal bone trauma and their percentages? 5

A
  1. Incudostapedial joint dislocation (most common - 82%)
  2. Complete incus dislocation (57%)
  3. Stapedial crural fractures (30%)
  4. Epitympanic ossicular fixation (25%)
  5. Malleus fracture (11%)
20
Q

Which ossicle is the least secure and most susceptible to shear force in temporal bone trauma?

A

Incus

21
Q

What is an indication and contraindication for exploratory tympanotomy and ossicular reconstruction in temporal bone trauma?

A

INDICATION:
- > 30dB CHL persistting > 2 months post injury (after hemotympanum resolves)

CONTRAINDICATION:
- Only hearing ear

22
Q

What is the most common site of facial nerve damage from temporal bone trauma, and list 3 reasons why this occurs?

A

Distal labyrinthine segment (narrowest segment) and Geniculate Ganglion

  1. Small size and lack of fibrous supporting tissue
  2. Traction between GSPN and Geniculate Ganglion (under higher tension and easier to snap)
  3. Watershed areas of vascularization - via the labyrinthine branch of the anterior inferior cerebellar artery [AICA] and the superficial petrosal artery (branch of middle meningeal from external carotid)

Vancouver notes says watershed area includes stylomastoid artery but Kevan’s note and other sources say the above

23
Q

What are five poor prognostic indications in traumatic facial nerve paralysis?

A
  1. Transverse temporal bone fractures
  2. Immediate onset of paralysis
  3. Complete paralysis/paresis
  4. Penetrating mechanism of injury
  5. Signs of proximal injury (e.g. loss of stapedial reflex - hyperacusis, taste change from chorda tympani injury, parasympathetic dysfunction of nose/lacrimal glands)
24
Q

Which patients may benefit from early surgical intervention in facial nerve injury following temporal bone injury? 4

A
  1. Immediate paralysis with no return of function and absent responses on EMG > 1 week
  2. Immediate paralysis with progressive decline on ENoG to >90% degeneration within 6 days of injury (need surgery within 14 days of injury)
  3. Immediate paralysis with CT evidence of significant temporal bone disruption, bony impingement, or obvious transection of fallopian canal
  4. Exploration at time of surgery for other reasons
25
Q

What are 3 indications for conservative treatment in facial nerve injury with temporal bone fractures?

A
  1. Delayed onset - documented normal facial nerve function after injury, regardless of progression
  2. Incomplete paralysis at presentation that doesn’t progress to complete
  3. Complete paralysis (either from outset or progression to) with < 90% degeneration on ENoG
26
Q

What are Crocodile Tears? Describe the pathophysiology with respect to temporal bone fractures.

A

Crocodile Tears = Bogorad’s syndrome

Definition: Tearing with salivation, due to synkinesis occurring with recovery from facial nerve palsy (most common Bell’s palsy followed by trauma)

Synkinesis = involuntary/undesirable facial movements or simultaneous movements that occur/associated with voluntary facial movements (due to nerve rewiring)

PATHOPHYSIOLOGY:
- Fibers cross innervate from LSPN to GSPN after trauma to the anterosuperior surface of the temporal bone (petrous apex)
- Has also been described as cross innervation of chorda and GSPN if injury is before the geniculate; if after geniculate thought to be LSPN

PATHWAY:
- Inferior salivatory nucleus –> CN IX –> Jacobsen’s nerve –> Lesser superficial petrosal nerve /// cross wires to GSPN /// –> Greater superficial petrosal nerve –> vidian nerve –> sphenopalatine ganglion –> Zygomaticotemporal branch of V2 –> Lacrimal gland

27
Q

What is the most common area of iatrogenic facial nerve injury in the temporal bone?

A

Tympanic segment

28
Q

What are 4 emergencies with middle and inner ear trauma?

A
  1. Brain herniation
  2. Massive hemorrhage - angio ± balloon occlusion
  3. Vertigo with penetrating injury
  4. Other neurologic deficits
29
Q

3 approaches to post-traumatic facial nerve repair from Temporal bone injury?

A
  1. Lateral to geniculate ganglion - transmastoid ± facial recess approach
  2. Medial to geniculate with no hearing - translabyrinthine approach
  3. Medial to geniculate with hearing - combination middle cranial fossa, transmastoid and transepitympanic (supralabyrinthine)

Otology & Neurotology (17 decks)

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