Physiology of acoustic blast injury

Introduction

Damage to the ear is the most common organ injury after exposure to blast overpressure (BOP). A blast injury occurs due to a rapid overpressurization force to the body. The middle and inner ear are particularly sensitive to sudden pressure changes and are therefore very susceptible to blast injuries. Blast injury to the ear may be caused by the detonation of high-order explosives (e.g., dynamite, nitroglycerine) that produce a supersonic, overpressurization shock wave, or by nonexplosive sudden pressure changes in the external auditory canal (EAC), such as a slap to the side of the head. These mechanisms generally cause a rapid increase in pressure within the EAC and can lead to a variety of middle and inner ear injuries. Patients with otologic damage after BOP often present with tympanic membrane rupture. Additional signs and symptoms may include ossicular chain dislocation, conductive, mixed or sensorineural heading loss, tinnitus, and dizziness/vertigo. ^, While it is not uncommon for tympanic membrane perforations and conductive hearing loss to improve spontaneously, a subset of patients continues to experience transient or permanent high-frequency sensorineural hearing loss (SNHL), suggestive of additional inner ear damage. In this chapter, we examine the anatomy and physiology of the ear as it relates to blast injury.

Background: normal anatomy and physiology of the ear

Sound waves travel along the EAC to reach the tympanic membrane (TM), which separates the external ear from the pneumatized middle ear ( Fig. 4.1A ). The tympanic membrane can be divided into four quadrants and is comprised of the pars tensa and the pars flaccida. The pars tensa, which makes up the majority of the drum, consists of three distinct layers—a lateral epithelial layer, a fibrous middle layer, and an inner mucosal layer. The pars flaccida, located superiorly between the anterior and posterior malleolar ligaments, lacks the fibrous layer and is as such less resistant to pressure changes. The middle ear contains the ossicular chain, specifically the three ossicles, malleus, incus, and stapes. The malleus attaches to the tympanic membrane and medially connects with the incus via the incudomalleolar joint. The incus interacts with the stapes through the incudostapedial joint, and the stapes footplate provides direct communication with the inner ear via the oval window ( Fig. 4.1A ). The ossicular chain acts as a lever, causing relative medial displacement of the stapes footplate at the oval window. The middle ear matches the lower impedance of sound waves in the air to the higher impedance fluid in the cochlea. This amplifying function has been described as middle ear gain, and the impedance matching is essential for the efficiency of air conduction. The vibratory area of the tympanic membrane is about 20 times greater than the area of the stapes footplate. This area ratio together with the mechanical lever effect especially from the malleus and incus achieves a middle ear gain of roughly 25–35 dB. Damage to the middle ear conductive pathway impairs the efficiency of sound conduction and consecutively can lead to conductive hearing loss. ^,

In the inner ear, transmitted sounds propagate as frequency-dependent travel waves through inner ear fluids along the turns of the cochlea, moving the basilar membrane and with it the organ of Corti (OC) ( Fig. 4.1B ). The cochlea is organized in tonotopic fashion, with high frequencies located at the base, and low frequencies located at the apex. Different frequencies result in a distinct peak of a traveling sound wave along the basilar membrane. Its movement creates localized shearing forces along the OC, which, through subsequent steps, initiate the process of mechanotransduction: Mechanical energy of the traveling wave is transformed into electrochemical energy at the apical surface of the inner hair cells within the OC. Stereocilia bundle movement leads to opening of ion channels, potassium influx, and subsequent depolarization of hair cells. Neurotransmitter release from ribbon synapses at the basal portion of inner hair cells stimulates bipolar afferent spiral ganglion neurons. An action potential is generated, and the signal is transmitted along the central auditory pathway in a tonotopic organization. Outer hair cells (OHCs) serve to amplify and tune the cochlear traveling wave through an additional active motile process.