Otitic barotrauma by Dr Manohar Suryawanshi ENT resident INHS Asvini, Mumbai

OTITIC BAROTRAUMA

Introduction

• Diving as a profession can be traced back more than 5000

years, yet diving-related disease was not described until Paul

Bert wrote about caisson disease in 1878.

• Diving barotrauma can present with: Pain in ear, face or mouth

and headaches to major joint pain, paralysis, coma and death

• Three major manifestations:

(1) Sinus or middle ear

(2) Decompression sickness

(3) Arterial gas emboli

Introduction

History

• Diving bell:

- Alexander the Great at the siege of Tyre in 323 Bc

• Modern diving bell:

- A form of caisson, was invented by John Smeaton in 1788

• SCUBA: self contained underwater breathing apparatus

- Invented by Emile Gagnon and Jaques Cousteau in 1943

• In 1897, Alt described middle and inner ear injuries caused by

compression and decompression in caisson workers

• Alt and Vail:

- Animal experiment

- Inner ear compression barotrauma was related to the failure of

middle ear pressure equalization

• Vail: also hypothesized that decompression injury was caused

by an effect on the inner ear by nitrogen bubbles

Definition

• Defined as an injury produced by mechanical forces caused by

a change of pressure in a gas-filled space.

• Otitic barotrauma: pathological conditions of the ear

induced by pressure changes.

• Pressure/volume relationships:

- Inverse relationship between the pressure of a gas and the

volume it occupies is described by Boyle's Law

• The pressure increase with depth is a linear relationship of

approximately 1 kPa for every 10 cm depth

• Descent in air from 5500 m to sea level represents a pressure

increase of only 0.5 atmospheres (50.5 kPa)

• When diving, the largest percentage change in gas volume

occurs during the first 10 metres of descent

• For aviators during the first 1000m of altitude

Ambient pressure change

• The external pressure is uniformly distributed over an object

• In a system which has no air spaces within it, this pressure is

transmitted equally throughout the structure

• Head-out immersion causes a significant squeezing of blood

volume from the lower limbs into the chest and into the head

causing an increasing cardiac output and raised intracranial

pressure and headaches respectively

• In the submerged diver, or aviator, the pressure is equally applied to

all body structures, there is no differential pressure across any

membranes or systems so function is essentially unchanged

• The exception is an air-filled cavity within the body

• Middle ear is a bony cavity, no distension or expansion is able to

take place


• Failure to equalize via the Eustachian tube -> negative middle

ear pressure

• Difference between the intraluminal vascular pressure and the

middle ear air pressure

• Oedema and even rupture of those vessels within the mucosal

lining will occur


• Physiological Consequences of compression (Descent):

• As the diver descends, the ambient pressure increases

• The middle ear pressure becomes increasingly negative

compared to the ambient pressure unless equalization via the

Eustachian tube takes place

• This occurs by the voluntary action of the tensor and levator

palati muscles opening the usually closed tube

• If Eustachian tube cannot be opened -> pressure equalization in

middle ear space, with that of the external pressure, cannot

occur

• Further descent -> resulting in a pressure differential across the

tympanic membrane, which is therefore pushed inwards by the

external water pressure

Descent:

• This stretching is perceived as a sensation of external pressure

and discomfort, which stimulates further attempts at

equalization

• Diver should return towards the surface

• If descent continues, then middle and inner ear barotrauma

Descent:

• The perception of the requirement to equalize occurs at a

maximum of 86 cm (2.6 ft) reflecting a pressure change of only

8.7 kPa (60 mmHg).

• At this pressure, if no equalizing manoeuvre -> increases the

transmural pressures, thus increasing transudation -> mucosal

congestion and oedema

• Continued descent results in 'Eustachian locking' at 13 kPa (90

mmHg), an equivalent depth of approximately 1.3 m (3.9 ft)

Descent:

• Levator palati muscles is insufficient to voluntarily overcome the

external closing pressures -> middle ear barotrauma

• If the pressure gradient across the tympanic membrane is large

and occurs before the middle ear fills with an effusion or blood,

then the tympanic membrane may rupture

Descent:

• Physiological consequences of decompressin (Ascent):

• During normal ascent, as the middle ear pressure exceeds that

of the ambient pressure, passive ventilation through the

Eustachian tube into the pharynx occurs.

• When flying, this normally occurs every 13.25 m (43.5 ft) of

ascent, regardless of the speed of decompression.

• If both Eustachian tubes are functioning correctly then the only

conditions experienced on ascent are decompression illness

• During a diver's descent mild middle ear barotrauma may occur

due to suboptimal Eustachian tube function

• To continue ascending -> positive middle ear pressure ->

outward bulging of the tympanic membrane

• Tympanic membrane is pushed outwards

• Inward force on the round window membrane

• Pressure gradient is increased further as the perilymphatic pressure,

reflecting the ambient pressure, has decreased with ascent.

• It is possible, therefore for perilymphatic fistulae to occur during this

phase of a dive.

Manifestations of otitic barotrauma divided into:

1. Compression injuries

a) External ear barotrauma

b) Middle ear barotrauma

c) Inner ear barotrauma

2. Injuries at stable pressure

3. Decompression injuries

A) External ear barotrauma

Clinical presentation

• Main symptom is of pain, increasing with depth

• The ear canal skin and tympanic membrane:

- hyperemic, petechial haemorrhages and even bleeding

B) Middle ear barotrauma

Clinical Features:

1. The initial symptom is the sensation of a blocked ear with a strong

desire to equalize

2. Otalgia, which worsens with increased compression

3. Minimal initial conductive loss (decreased compliance)

to the Larger conductive loss (due to damage to the stapes foot

plate, incus dislocation and fractured malleus handle)

4. Tympanic membrane perforation

5. Caloric vertigo - sudden ingress of water into the middle ear

Tympanic membrane appearance in middle ear barotrauma (Modified

Teeds grading):

Grade Symptoms and signs

O Symptoms, no signs

1 Redness and retraction

Grade Symptoms and signs

2 Intratympanic membrane haemorrhage

3 Gross tympanic membrane haemorrhage

4 Haemotympanum

5 Perforation

• Equalization tests:

1. Valsalva's manoeuvre - poor predictive test for potential

barotrauma

2 Toynbee's test (positive predictive value of 25 percent)

3 Nine-step Eustachian tube test (positive predictive value, 25 percent;

negative predictive value, 75 percent).

4. Combining the nine-step test with Toynbee's test -Reliable (100

percent)

5. Sonotuberometry and tubotympanometry: accurately predict

• Degree of mastoid pneumatization:

- Pneumatization of greater than 34.7 cm2-> decreased

barotrauma

- Pneumatization less than 13.6 cm2 -> inceased

barotrauma

Treatment of ME Barotrauma

• Treatment regimen (on basis of 3 level clinical classification of

severity):

• Type 1. symptoms, but no (or minimal) signs

- requires no specific treatment

Type 2. significant signs, but no perforation

- conservative with oral or topical nasal decongestants

Type 3. with perforation

- initial observation

- myringoplasty (fail to heal)

Prevention of middle ear barotrauma

Medical:

1. Nasopharyngeal irradiation

- Poor success rates and radiation induced tumors, stopped

this practice

2. Topical nasal decongestants and oral pseudoephedrine

• 3. Nasal balloon inflation (auto-Politzerization) using Otovents

Surgical:

• Myringotomies with or without the insertion of ventilation

tubes

Diving and flying after Middle ear surgery:

• Restriction of any activity for at least six weeks

• Stapedotomy technique:

- As the potential consequences of a perilymphatic fistula when

diving are so extreme, postoperative wait of 12 months is

recommended

Caloric Vertigo:

• Rupture of tympanic membrane

• Severe acute caloric vertigo

• Colder the water, more severe the effect

• Vertigo is self-correcting if caloric stimulus is removed

Inner ear barotrauma

• Two mechanisms:

a) Implosive

b) Explosive

a) Implosive mechanism:Inner ear barotrauma

b) Explosive mechanism Inner ear barotrauma

Classification:

1. Inner ear haemorrhage

2. Labyrinthine membrane tears

3. Perilymphatic fistula


• Inner ear haemorrhage:

- Transient, or minimal, vestibular symptoms

- Mild to moderate sensorineural hearing loss

- Good recovery


• Labyrinthine membrane tears:

- Vertigo and tinnitus

- Characteristic low frequency hearing loss

- Inner ear damage: haemorrhage around Reissner's and the

round window membranes

- Rupture of the utricle and saccule


• Temporal bone:

- Reissner's membrane rupture

• In normally ventilated ears, the inner ear is more susceptible to

decompression trauma

• Implosive forces to the inner ear causes middle ear overpressure

(ascent with a locked ET), than compression (descent)


Perilymphatic fistulae

• Sudden onset of vertigo

• Sensorineural hearing loss

• Tinnitus

• Positional nystagmus

• Tullio phenomenon

• Tympanic membrane: signs of middle ear barotrauma

• Nystagmus usually towards the opposite side

• Romberg's test is normal in more mild cases

• Unterberger's step test

• Side-step test


• Inner ear decompression sickness:

• Commercial and military divers who breathe a compressed

mixture of helium and oxygen

• Decompression (ascent), or shortly after surfacing from a dive

• Hyperbaric chamber for recompression


Treatment:

• Initial conservative approach (bed rest for 05 days)

• Exploration reserved for:

(1) Those with progressive hearing deterioration observed

on daily, or more frequent, audiometry

(2) If the vestibular symptoms fail to improve after 05 days

(3) Failure of complete resolution after one month


• Moderate to Severe hearing loss:

- Emergency exploration in severe acute cases with both a

significant hearing loss and vertigo (40 dB HL)


• Minimal Hearing loss:

- Mild vestibular symptoms and hearing losses ( high frequency only,

or < 20 dB HL)

- Initial conservative (bed rest with elevation of the bed head to 30-40

degree)


• Surgical exploration:

- Daily audiometry

- Subjective deterioration

- Vestibular symptoms


• Mild to moderate hearing loss:

• Persistant vestibular symptoms without hearing loss:

- Conservatively for upto 04 weeks

- Hearing loss with vestibular component presenting more than

24 hours following the incident -> conservative


• Surgical exploration:

- Earlier the presentation with hearing loss after the event, and

worse the vestibular component-> urgent surgery

- Evidence of deteriorating hearing

- if vestibular symptoms and hearing loss persist (exploration

after 05 days)


• Surgery for perilymphatic fistula:

• Exploratory tympanotomy

- Look at the round, oval windows and Eustachian tube orifice

for a source of the leak

- Tissue plug and absorbable middle ear packing material

- If no fistula is observed, then tissue graft in the round window

and over the foot plate

- Vein (sticky nature of its adventitial surface)

- Fluid collection for beta 2-transferrin

Injuries at Stable Depth

High-pressure nervous syndrome:

Clinical presentation:

• General dizziness and tremors

• Ataxia and myoclonus

• Sudden onset of vertigo and nausea with nystagmus

has been reported as part of this syndrome.

• Permanent vestibular damage has been described, but there is

no hearing loss

• Prevention:

- Minimized by ensuring slow descents and by avoiding inert gas

changes at depth

High-pressure nervous syndrome

• If symptoms are encountered when a helium-oxygen mix

is changed to air during ascent, then the treatment is to

recompress back on helium-oxygen

High-pressure nervous syndrome

Decompression injuries

• Alternobaric vertigo:

• Condition of asymmetrical middle ear overpressure stimulation

occurring in both divers and aircrew.

• Pathoetiology:

- On ascent, failure of equalization due to minor middle ear

congestion and oedema -> relatively higher pressure in one middle

ear than the other.

• Condition occurs on ascent or within two minutes of surfacing.

• Episodes are short lived, with a maximum duration of ten

minutes.

• Divers may also describe a tumbling sensation or a tilting of

their surroundings

Alternobaric vertigo

Barotraumatic facial palsy

• Patho-aetiology:

• Pressure-induced neuropraxia (most widely accepted

explanation for transient unilateral facial palsy .

• Dehiscence of the facial nerve in its intramastoid portion (0.5 to

57%)

• Animal studies have demonstrated that blood flow in the vasa

nervora of the facial nerve decreases if increased middle ear

pressure is transmitted through a dehiscence of the facial canal

• Alternative hypothesis:

- In a non-dehiscent facial canal, pressure may be transmitted

through the fenestra of the chorda tympani.

Persistent palsy:

• Myringotomy

• If rapid resolution does not occur, then oral steroids should be

considered.

• A persisting palsy should be investigated and treated as for a

decompression illness.

THANK YOU

Otitic barotrauma by Dr Manohar Suryawanshi ENT resident INHS Asvini, Mumbai

Health & Medicine

Transcript of Otitic barotrauma by Dr Manohar Suryawanshi ENT resident INHS Asvini, Mumbai