Diving Injuries to the Inner Ear

Abstract

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases. 2) Vestibular end-organ injuries have been noted in three divers after sudden changes in inspired inert gases at a stable deep depth. They are postulated to result from transient intralabyrinthine osmotic pressure differences, or from bubble formations at labyrinthine tissue interfaces occurring with the counter-diffusion of the two dissolved inert gases at high partial pressures. Such injuries should be preventable by avoiding changes in inert gases at deep depths. 3) Inner ear injuries can be the major or only manifestation of decompression sickness. In a series of 23 such cases, a significant correlation exists between prompt recompression, relief of symptoms, and lack of residual deficits. The management of otologic decompression sickness is discussed. 4) Loud noise has been noted during helmet and chamber diving and has been associated with temporary threshold shifts in helmet divers. Appropriate damage risk criteria for noise exposure in compressed gas environments are needed, and potentially damaging noise exposures should be avoided.