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We present a rare case in which barotrauma led to fracture of the stapes footplate and perilymph fistula, resulting in sudden severe sensorineural hearing loss and tinnitus. Surgical repair in this case resulted in excellent hearing recovery. The aetiology and management of inner ear barotrauma and stapes injury is discussed. We believe that early exploration and repair of suspected perilymph fistulae optimises hearing recovery.

Traumatic endolymphatic hydrops is an accumulation of endolymph in the cochlear duct caused by traumatic insult. The causative mechanisms are: (1) fistulization of the bony labyrinth, which causes a disturbance in the normal perilymph-endolymph pressure relationship; (2) direct injury to the membranous labyrinth, which may be just a collection of fluid in the cochlear duct from irritation, resulting in endolymphatic hydrops that may not be progressive and may subside in a short period of time after injury and hearing loss may occur; and (3) injury to the endolymphatic fluid drainage system, including a temporal bone fracture in which the fissure happens to extend through the vestibular aqueduct, causing fibro-osseous blockage of the endolymphatic duct and surgical injury to the saccule with obstruction of the longitudinal flow of endolymph, resulting in endolymphatic hydrops that may be delayed in onset and is usually persistent. The diagnosis of traumatic endolymphatic hydrops is made by a history of trauma, such as barotrauma, a blow to the head, or perhaps a previous ear operation, such as stapedectomy; the presence of typical symptoms of endolymphatic hydrops, including fullness, tinnitus, fluctuant hearing loss, and episodic vertigo; and an elevated negative summating potential and an increased summating potential:action potential ratio by electrocochleography. Three patients are presented to demonstrate this clinical entity.

The case against the occurrence of spontaneous perilymphatic fistulas is presented. Electrophysiologic findings both in animals and in man suggest that small holes in either the round or oval window are not associated with any significant hearing loss. Removal of perilymph may cause some changes in the electrocochleogram that can be reversed when the perilymph is replaced. Tympanotomy surgery, especially when performed with the injection of local anesthetic solutions may result in transudates in the middle ear that are difficult to differentiate from perilymph leaking out from the inner ear. Perilymphatic fistulas were excluded by performing a posterior myringotomy under general anesthesia in 162 congenitally deaf ears. If fluid was present it was suctioned, and if no change occurred on the intraoperative electrocochleogram, it was concluded that no fistula existed. Based on the electrophysiologic findings and the clinical observations in over 240 ears, it was concluded that spontaneous perilymphatic fistulas do not exist. The author accepts that perilymphatic fistulas occur after surgery, especially after stapedectomy, and that they can occur after head injury or barotrauma. However, these should heal readily; persistent or intermittent fistulas are an otologic rarity.

The association between diving, barotrauma, and the production of perilymphatic fistula has been known for almost 20 years. Forty-eight cases of round and oval window fistulas following diving have been reviewed and essentially corroborate previous findings. Any patient with a history of diving and subsequent sensorineural hearing loss within 72 hours should be suspected of having a round or oval window perilymphatic fistula and surgical exploration and closure of the fistula should be undertaken. Patients who have a loss of hearing, vertigo, nausea, or vomiting following a decompression dive should be re-compressed and if symptoms do not clear, exploration should be performed. Surgical treatment should be executed as soon as possible after the diagnosis is suspected for the best possible results.

In the course of exploratory tympanotomies we have several times come across air bubbles leaking with perilymph. The fact prompted the hypothesis that in some cases of perilymphatic fistulas, air bubbles could enter the perilymphatic space from the fistula of the inner ear membrane and cause acute, reversible, profound sensory hearing loss. The experimental study described here was designed to test this hypothesis on guinea pigs. Experiments showed that sudden elevation of middle ear pressure by artificial means caused air bubbles to appear in the scala tympani even at a pressure level of 400 mm H2O. It also proved that air bubbles entered the perilymphatic space through the ruptured round window membrane without damaging Corti's organ or the membranous structure of the cochlea. Sequential recording of the action potential revealed that air bubbles induced acute, reversible, and profound hearing loss of cochlear origin, probably by disturbing the propagation of traveling waves of the perilymph.

Tympanotomy is routinely performed in our institution to control the round window membrane for patients with recurrent sudden deafness, with Meniere-like attacks, and those with Meniere's disease. In a large number of these patients, especially those with vertigo, perilymph fistula has been diagnosed. Most patients are free of attacks after the fistula has been closed, and in those with a short history of illness, hearing can become normal. In the future, closure of the round window membrane should be considered an important procedure in the treatment of inner ear dysfunctions.