The structures of the middle ear serve to transform incoming sound waves into electrochemical energy and send it to the hearing centers of the brain.
The tympanic membrane separates the external auditory canal from the middle ear.
Structurally, the TM is made of a flexible membrane that vibrates in response to variations in air pressure.
These vibrations, ie., sound waves, are in turn transmitted and augmented by a set of three ossicles into the inner ear as hydraulic energy.
The cochlea of the inner ear contains hair cells that, when stimulated by the incoming hydraulic energy, sends these transduced impulses to the brain.
Blast Injury of the Ear:
During the primary blast wave, a large amount of energy is released in a relatively short amount of time.
A shock wave of overpressure travels through the air at a velocity greater than the speed of sound, followed by a region of gas flow.
This results in a short positive-pressure phase and a relatively long negative pressure phase.
This variation in blast overpressurization and underpressurization versus time can be plotted as a Friedlander curve.
The extent of damage from the primary blast injury is usually inversely proportional to the distance away from the blast.
Along with distance, orientation of the ear canal plays a significant role in blast injury of the ear.
Experiments have shown that blast waves that are side on have lower measured peak overpressures at the tm.
Therefore, depending on whether the blast wave meets the auditory canal side on or directly will determine the amount of energy imparted and, subsequently, the likelihood of injury.
Another consideration of blast injury to the ear that needs to be taken into account is the environment.
Open space and closed space blast injuries differ in many aspects.
Due to the physics of blast waves, location within an environment may change the severity of injury regardless to distance.
Adjacent building, walls, staircases, and other structures will alter the blast wave physics by numerous reflections and rarefactions.
The heating of gases within this space may also result in a sustained period of positive pressure, therefore, prolonged injury (4).
The Outer Ear:
The pinna and external auditory canal are unlikely to be damaged by the primary blast wave, but, more from secondary blast injuries such as shrapnel and flying debris.
Since the outer ear has a good vascular supply, most injuries will heal well.
It is generally accepted that repair with minimal cleaning gives good cosmetic results.
Large pieces of cartilage should be preserved to maintain the contour of the ear.
If degloving has occurred, it may be necessary to bury the cartilage under a post –aural skin flap with ENT/plastics repair at a later date.
Prophylactic antibiotics should be considered to reduce the incidence of perichondritis (4).
When the primary shock wave reaches the end of the external auditory canal, it stretches and displaces the drum medially (4).
Depending on the force of the blast, the tympanic membrane may become perforated in one or more places.
These injuries to the tympanic membrane are often temporary but may remain persistent without treatment.
The tympanic membrane is the most frequently injured structure during an explosion.
Often, very little pressure is needed to induce tympanic membrane rupture.
During WWII, the ear was the organ most affected by blast and often the only one (3).
Records show that of 36,000 patients treated at a Paris hospital, 5.8% were otologic injuries.
Of those patients with otologic injuries, 36.7% were tm perforations (9).
A small increase in pressure, as little as 5 psi, can rupture the human eardrum (2).
Rupture pressure was first measured in humans by Zalewski in 1906.
By gradually increasing pressure applied to the ear canal with a bicycle pump, the mean rupture pressure was measured to be 1.59 atm (6).
Another study performed on cadavers by Jensen and Bonding involved delivering pressure to the ear via an electrical pump. Rupture pressure measured by a manometer was determined to be 1.2 atm, with a wide range of 0.5 to 2.1 atms.
These studies, along with other experiments measuring the rupture pressure of different species, show that relatively little pressure is needed to perforate the tm, but, a large variation in rupture pressure was evident among subjects.
In contrast, pressure gradients of 56 to 76 psi (3.8 to 5.2 atm) are needed to cause damage to other organs (2).
TM Rupture Symptoms
Most of the time, the tm tends to spontaneously heal.
Perforation symptoms may include
whistling sounds during sneezing or nose blowing,
and increased susceptibility to infections when the ear canal is exposed to water.
Ottorhea, which may occur in acute and chronic tm perforations, confirms both perforation and infection.
Perforations uncomplicated by infection or cholesteatoma are usually not painful.
Presence of pain should alert the physician to a concurrent disease process (1).
Anatomically, the tympanic membrane has two distinct zones.
The first is the pars flaccida.
The second, the pars tensa, is larger and tends to be where most of the injury to the tm occurs.
The pars tensa zone contains a layer of squamous epithelium on the outside and a mucosal layer on the inside.
Management of tympanic membrane perforations depend on the time after the blast injury, the size, and the location of the perforation.
Most tm perforations are diagnosed during routine otoscopy, although, smaller perforations may require the use of an otomicroscope.
Always perform audiometry tests to differentiate between perforations and possible ossicular damage and to protect oneself against claims of treatment induced hearing loss (1).
Medical management of perforations is usually in controlling the otorrhea and avoiding contamination of the middle ear with water.
Systemic antibiotics are sometimes used to treat infections due to the ototoxicity of some topically applied eardrops.
If topical eardrops are prescribed for infections secondary to a tympanic membrane perforation, a less toxic alternative should be substituted as soon as drainage and edema begin to subside (1).
If initial medical management does not work, there are different surgical alternatives to tympanic membrane repair.
The simplest type of repair involves debridement of the perforation edges.
Placement of a patch, whether from a graft, cigarette paper, or synthetic composition may successfully close the tm perforation.
In one study, Kronenberg reviewed 147 patients with 210 combined tympanic membrane perforations after blast injuries from 1967-1986.
Injury size was graded on a scale of 1-4, with 4 being the largest on the scale of perforations.
According to the study, the rate of spontaneously healing was 73.8%, with most of the healing occurring within 10 months.
The rate of spontaneously healing was inversely related to the size of the perforation.
If a paper patch was used, it was found to facilitate the rate of spontaneous closure.
The risk of developing cholesteatomas was confined to patients who had persistent tm perforations longer than 10 months.
Therefore, tympanoplasty was recommended for perforations that do not heal after 10 months with conservative treatment and paper patching.
Aside from tympanic membrane damage, there may be damage to the ossicles of the middle ear.
Different studies have reported ossicular damage ranging from 4-33% of perforated tms.
The most common injury that occurs is the disruption of the incudomalleolar joint (4).
Incidentally, disruption of the ossicles may absorb some of the incoming energy of the blast wave, sparing the structures of the inner ear.
When the overpressure of the primary blast wave ruptures the tympanic membrane, it sends small fragments of the squamous epithelium into the middle ear cavity.
These cells may still be viable and grow into masses, called cholesteatomas, which can infect or erode ossicles and, in severe cases, extend intracranially.
Complications of cholesteatomas include nerve damage, deafness, and vertigo.
Careful surgical debridement is recommended for removal with close follow up as 10-20% of cholesteatomas recur.
The Inner Ear:
Immediately following a blast injury, patients may experience short lived hearing loss and tinnitus.
Although the hearing loss may be transient, lasting only for a few hours, some may experience extended hearing loss.
For a segment of patients, there is permanent damage, usually with symptoms of hearing loss in high tones and tinnitus.
Permanent hearing deficits usually correspond with damage to the organ or Corti.
More specifically, the blast overpressure induces a tearing of the sensory cells from their cell attachments on the basilar membrane or significant displacement of the basilar membrane itself(5).
Even after healing, the mechanical properties of the basilar membrane may be altered by scar tissue and may affect surrounding cells resulting in hearing loss or profound decrease in auditory acuity.
Labrinthine damage may also occur after blast injuries resulting in complaints of vertigo.
Careful evaluation by an ENT surgeon is indicated to rule out perilymph leak as the cause of these vertiginous symptoms.
Management of Blast Injury to the Ear:
Treatment of patients after a primary blast injury of the ear involves careful initial screening and appropriate follow up.
All patients on arrival to a medical facility after blast injury should have a quick screening exam to look for perforated tympanic membranes.
Although serious blast injuries can occur in the absence of tympanic membrane rupture, an unruptured tm in the absence of other symptoms such as dyspnea, respiratory distress, and acute abdominal pain may rule out serious injury (2).
Patients with ruptured tms should have a chest x-ray and should be monitored for at least 8 hours.
As previously discussed, tm rupture should be treated conservatively.
Patients should avoid probing or getting water into the ear canal.
If debris is present, antibiotics should be started to help clear debris and debridement/suction may be warranted in the ENT department.
Since there are many complications to perforated tms, ossicular damage, and inner ear damage, all patients should have audiometry assessment and close ENT follow-up.
References and Selected Readings regarding BLI:
1) Patterns of global terrorism 2001. United States Department of State. May 2002. United States Department of State website. Available at: http://www.state.gov/documents/organization/10319.pdf. Accessed 4 February 2005.
2) Patterns of global terrorism 2002. United States Department of State. April 2003. United States Department of State website. Available at: http://www.state.gov/documents/organization/20177.pdf. Accessed 4 February 2005.
3) Patterns of Global Terrorism 2003. United States Department of State. April 2004. United States Department of State website. Available at: http://www.state.gov/documents/organization/31912.pdf. Accessed 4 February 2005.
4) Terrorism 2000/2001. United States Department of Justice, Federal Bureau of Investigation, Counterterrorism Division. Publication #0308. Federal Bureau of Investigation website. Available at: http://www.fbi.gov/publications/terror/terror2000_2001.htm. Accessed 4 February 2005.
5) Gadson LO, Michael ML, Walsh N (eds). FBI Bomb Data Center: 1998 Bombing Incidents, General Information Bulletin 98-1. US Department of Justice, Federal Bureau of Investigation. 1998.
6) Wightman JM, Gladish SL. Explosions and blast injuries. Annals of Emergency Medicine. 2001; 37(6): 664-678.
7) Horrocks CL Blast Injuries: Biophysics, pathophysiology, and management principles. J R Army Med Corps 2001;147:28-40.
8) Cullis, IG. Blast waves and how they interact with structures. J R Army Med Corps 2001;147:16-26.
9) Langworthy MJ, Sabra J, Gould M. Terrorism and blast phenomena: lessons learned from the attack on the USS Cole (DDG67). Clinic Orthop. 2004; 422: 82-87.
11) Yetiser S and Ustun T. Concussive blast-type aural trauma, eardrum perforations, and their effects on hearing levels: an update on military experience in Izmir, Turkey. Mil Med. 1993; 158 (12):803-806.
12) Mayorga MA. The pathology of primary blast overpressure injury. Toxicology. 1997; 121:17-28.
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27) Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus open-air bombings-a comparative study of injuries in survivors of open-air versus confinedspace explosions. J Trauma. 1996; 41: 1030-1035.
28) Hirshberg B, Oppenheim-Eden A, Pizov R, et al. Recovery from Blast Lung Injury: One-Year Follow-up. Chest. 1999; 116(6): 1683-1688.
29) Frykberg ER, Tepas JJ, Alexander RH. The 1983 Beirut airport terrorist bombing: injury patterns and implications for disaster management. Am Surg. 1989; 55: 134-141.
30) Irwin RJ, Lerner MR, Bealer JF, Mantor PC, et al. Shock after blast wave injury is caused by a vagally mediated reflex. J Trauma. 1999; 47(1): 105-110.
31) Frykberg, ER. Medical management of disasters and mass casualties from terrorist bombings: how can we cope? J Trauma. 2002; 53:201-212.
32) Stuhmiller JH, Ho KHH, Vander Vorst MJ, et al. A model of blast overpressure injury to the lung. J Biomech. 1996; 29(2):227-234.
33) Stuhmiller JH. Biological response to blast overpressure: a summary of modeling. Toxicology. 1997; 121: 91-103.
34) Zhang J, Wang Z, Leng J, Yang Z. Studies on lung injuries caused by blast underpressure. J Trauma. 1996; 40 (3 supplement): s77-s80.
35) Elsayed NM, Gorbunov NV. Interplay between high energy impulse noise (blast) and antioxidants in the lung. Toxicology. 2003; 189(1-2):63-74.
43) Lavonis E. Blast injuries. Emedicine website. Available at: http://www.emedicine.com/emerg/topic63.htm. Accessed 4 February 2005.
44) Gorbunov NV, McFaul SJ, Van Albert S, et al. Assessment of inflammatory response and sequestration of blood iron transferrin complexes in a rat model of lung injury resulting from exposure to low-frequency shock waves. Crit Care Med. 2004 Apr; 32(4): 1028-34.
45) DePalma RG, Burris DG, Champion HR, Hodgson MJ. Blast Injuries. N Engl J Med 2005;352:1335-42. Data taken from http://www.bt.cdc.gov/masstrauma/pdf/blastlunginjury.pdf
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