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Otitic barotrauma by Dr Manohar Suryawanshi ENT resident INHS Asvini, Mumbai
- 1.
- 2. Introduction • Diving asa 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
- 4. • Three majormanifestations: (1) Sinus or middle ear (2) Decompression sickness (3) Arterial gas emboli Introduction
- 5. 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
- 6. • 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
- 7. • Vail: alsohypothesized that decompression injury was caused by an effect on the inner ear by nitrogen bubbles
- 8. Definition • Defined asan 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.
- 9. • 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
- 11. • Descent inair 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
- 12. 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
- 13. • In thesubmerged 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 Ambient pressure change
- 14. • Failure toequalize 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 Ambient pressure change
- 15. • Physiological Consequencesof 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
- 16. • If Eustachiantube 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:
- 17. • This stretchingis 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:
- 18. • The perceptionof 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:
- 19. • Levator palatimuscles 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:
- 22. • Physiological consequencesof 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.
- 23. • If bothEustachian 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
- 24. • Tympanic membraneis 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.
- 25. Manifestations of otiticbarotrauma 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
- 26. A) External earbarotrauma
- 27. Clinical presentation • Mainsymptom is of pain, increasing with depth • The ear canal skin and tympanic membrane: - hyperemic, petechial haemorrhages and even bleeding
- 28. B) Middle earbarotrauma 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)
- 29. 4. Tympanic membraneperforation 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
- 30. Grade Symptoms andsigns 2 Intratympanic membrane haemorrhage 3 Gross tympanic membrane haemorrhage 4 Haemotympanum 5 Perforation
- 32. • 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)
- 33. 5. Sonotuberometry andtubotympanometry: accurately predict • Degree of mastoid pneumatization: - Pneumatization of greater than 34.7 cm2-> decreased barotrauma - Pneumatization less than 13.6 cm2 -> inceased barotrauma
- 34. Treatment of MEBarotrauma • 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
- 35. Type 3. withperforation - initial observation - myringoplasty (fail to heal)
- 36. Prevention of middleear barotrauma Medical: 1. Nasopharyngeal irradiation - Poor success rates and radiation induced tumors, stopped this practice 2. Topical nasal decongestants and oral pseudoephedrine
- 37. • 3. Nasalballoon inflation (auto-Politzerization) using Otovents Surgical: • Myringotomies with or without the insertion of ventilation tubes
- 38. Diving andflying 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
- 39. 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
- 40. Inner ear barotrauma •Two mechanisms: a) Implosive b) Explosive
- 41. a) Implosive mechanism: Innerear barotrauma
- 42.
- 43. b) Explosive mechanismInner ear barotrauma
- 44. Classification: 1. Innerear haemorrhage 2. Labyrinthine membrane tears 3. Perilymphatic fistula Inner ear barotrauma
- 45. • Inner earhaemorrhage: - Transient, or minimal, vestibular symptoms - Mild to moderate sensorineural hearing loss - Good recovery Inner ear barotrauma
- 46. • Labyrinthine membranetears: - 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 Inner ear barotrauma
- 47. • 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) Inner ear barotrauma
- 48. Perilymphatic fistulae • Suddenonset of vertigo • Sensorineural hearing loss • Tinnitus • Positional nystagmus • Tullio phenomenon
- 49. • 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 Perilymphatic fistulae
- 50. • Inner eardecompression 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 Perilymphatic fistulae
- 51. Treatment: • Initial conservativeapproach (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 Perilymphatic fistulae
- 52. • Moderate toSevere hearing loss: - Emergency exploration in severe acute cases with both a significant hearing loss and vertigo (40 dB HL) Perilymphatic fistulae
- 53. • Minimal Hearingloss: - 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) Perilymphatic fistulae
- 54. • Surgical exploration: -Daily audiometry - Subjective deterioration - Vestibular symptoms Perilymphatic fistulae
- 55. • Mild tomoderate 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 Perilymphatic fistulae
- 56. • 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) Perilymphatic fistulae
- 57. • Surgery forperilymphatic fistula: • Exploratory tympanotomy - Look at the round, oval windows and Eustachian tube orifice for a source of the leak
- 58. - Tissue plugand 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
- 59. Injuries at StableDepth 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.
- 60. • Permanent vestibulardamage 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
- 61. • If symptomsare 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
- 62. Decompression injuries • Alternobaricvertigo: • 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.
- 63. • Condition occurson 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
- 64. 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%)
- 65. • Animal studieshave 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.
- 66. 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.
- 67.
Editor's Notes
- #4 Caissons are bells that are pressurized to keep the water out, enabling workers to work for many hours at depth , caisson disease were noted among bridge workers after finishing their shifts underwater and coming back to the surface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the joints or abdomen. severe back pain that left them bent over-> bends By N2 bubbles in body at deep pressure
- #8 nitrogen bubbles: obstruction in the internal auditory artery system
- #9 slap injuries , flying and subaqua diving, water skiing, high board diving and from blast injuries
- #10 relative bubble volume decrease experienced with increased pressure
- #13 If a large vein, e.g. the internal jugular, has pressure applied from the outside then, provided that the whole body is submerged, it will transmit this pressure onwards.
- #16 EAC separated from the middle ear by TM, ET connects middle ear cavity with the nasopharynx 2. Nasopharynx is filled with inspired air from a compressed air cylinder via a regulator during breathing. This air pressure is equilibrated by the regulator in the mouthpiece to be equal with the ambient external pressure, provided the diver continues to breath normally.
- #18 Equalization should be done
- #20 sudden influx of cold water into the middle ear may result in unequal thermal stimulation inducing a rigorous caloric vertigo.
- #25 traction force is applied to the oval window via the ossicles.
- #27 occurs when a pocket of air is trapped within the external auditory meatus. This may be because of cerumen, earplugs, foreign bodies or exostoses, air-containing space that can change in volume in response to changes in ambient pressure. During descent, the volume of this space decreases causing the tympanic membrane to bulge outward
- #33 nine-step tympanometry : 1. The tympanogram records resting middle-ear pressure. 2. EAC pressure is increased to +200 mm H2 O with medial deflection of TM and a corresponding increase in middle-ear pressure. The subject swallows to equilibrate ME overpressure. 3. While the subject refrains from swallowing, EAC pressure is returned to normal, thus establishing a slight negative ME pressure (as the TM moves outward). The tympanogram documents the established ME underpressure. 4. The subject swallows in an attempt to equilibrate negative ME pressure. If equilibration is successful, airflow is from the nasopharynx to the middle ear. 5. The tympanogram records the extent of equilibration. 6. EAC pressure is decreased to -200 mm H2 O, causing a lateral deflection of the TM and a corresponding decrease in ME pressure. The subject swallows to equilibrate negative ME pressure; airflow is from the nasopharynx to the middle ear. 7. The subject refrains from swallowing while EAC pressure is returned to normal, thus establishing a slight positive pressure in the middle ear as the TM moves medially. The tympanogram records the overpressure established. 8. The subject swallows to reduce overpressure. If equilibration is successful, airflow is from the middle ear to the nasopharynx. 9. The final tympanogram documents the extent of equilibration.
- #38 Surgical: for flying, This procedure is clearly contraindicated for diving
- #40 1 asymmetric exposure to cold water 2. Vomiting may occur under water, perhaps necessitating the removal of the regulator from the mouth (although modern regulators are designed to enable some vomiting to take place without their removal)
- #41 Failure of equalization of the middle ear pressure on the affected side. Sudden, large pressure changes in the middle ear can be transmitted to the inner ear, resulting in damage to the inner ear. This can cause severe vertigo and even deafness
- #42 Clearing of the middle ear in descent. Inward bulging TM->, ossicles toward the inner ear at the oval window-> pressure wave through the inner ear and outward bulging of the round window If forceful Politzer maneuver: Inflation of ET and tympanum by forcing air into the nasal cavity at swallowing. and ET suddenly opens,->a rapid increase in middle ear pressure ->ossicles to suddenly return to normal positions, causing the round window to implode.
- #44 attempts clear a blocked middle ear by Politzer maneuver and ET blocked and locked, a dramatic increase in ICT. Since the fluids surrounding the brain communicate freely with the inner ear fluids, this pressure may be transmitted to the inner ear-> sudden rise in the inner ear pressure -> round or oval window membrane to explode.
- #47 Siimilar to Acute Meniere's disease attack,
- #49 perilymphatic fistula should be suspected in an otherwise healthy ear (or in one with evidence of middle ear barotrauma) if there is a SNHL of rapid onset, constant Dysequilibrium, symptoms of a chronic perilymphatic fistula. Dysequilibrium which worsens, or changes to momentary vertigo when performing manoeuvres which increase the intracranial (and hence perilymphatic) pressure
- #50 Side step test: eyes closed, the patient takes two consecutive broad steps sideways, and then stops with both feet together. sway or overshoot in the same direction as the steps were taken is regarded as a positive result, the affected ear being on the side towards the direction of movement.
- #51 1. IEDCS is an injury that closely resembles inner ear barotrauma 2. contrast, barotrauma most often occurs during compression (descent) 3. recompression in ME and Inner Bro cause further middle and inner ear barotrauma. Conversely, not recompressing a patient with a decompression illness may result in permanent cochleovestibular damage, further progression of the decompression illness symptoms and even death.
- #52 Treatment options are centred on hearing and balance preservation
- #54 to minimize the intracranial, cerebrospinal fluid, and hence perilymphatic, pressures. Raising the intracranial pressure by coughing, straining, vomiting or performing Valsalva's manoeuvre should be avoided
- #55 may not have had fistulae, but intralabyrinthine pathology
- #56 if after five days there has been no hearing improvement and if any vestibular symptoms persist (or at any time at the first sign of further hearing deterioration), then a tympanotomy is recommended.
- #59 confirmatory test for the presence of perilymph 2. If the tympanotomy then it is probably unwise to perform ossicular surgery at the same procedure ->cochlear concussion due to minor further trauma. 3. Repair of TM can be performed at the time, but ossicular surgery should be staged
- #60 High-pressure nervous syndrome occurs when divers are, exposed to extremely high pressures tremors (both postural and intentional hands and even of the whole body) which may progress, with increasing pressure
- #63 usually occurs in those who describe unilateral equalization problem condition occurs on ascent or within two minutes of surfacing.
- #65 given to a facial nerve palsy occurring as a result of high middle ear pressure during ascent.
- #66 Both would explain the transient nature of the condition, as the blood flow would rapidly return to normal when the middle ear pressure is relieved.
- #67 painful bulging membrane