Functional Eustachian Tube Obstruction Research Articles

Prevention of Otitis Media With Effusion by Repeated Air Inflation in a Monkey Model

To test the following hypotheses that (1) middle ear (ME) air inflation prevents the development of otitis media with effusion in a monkey model of functional eustachian tube obstruction, and (2) ME inflation treatment of otitis media with effusion can cause artifactual clinical improvements due to fluid displacement from the tympanum to the adjacent airspaces. Randomized controlled trial. Twelve cynomolgus monkeys. Eustachian tube dysfunction was induced by botulinum paralysis of the right tensor veli palatini muscle in all monkeys. Before and on study days 9, 15, and 21 after paralysis, the presence or absence, and distribution of ME effusion were documented using magnetic resonance imaging (MRI). Right and left ears were examined twice daily for 21 days using tympanometry, and right ME air inflation (n = 6 ears) or sham inflation (n = 6 ears) was done immediately after those examinations if the ME pressure was -100 mm H2O or less. On 10 of the scheduled MRI evaluations, the MRI was repeated immediately after an inflation to document the possible redistribution of fluid within the ME caused by the maneuver. Middle ear pressure remained within normal limits for the follow-up period in 11 of the 12 nonparalyzed left ears, in none of the 6 sham-inflated right ears, and in 3 of the 6 air-inflated right ears. Three air-inflated right ears developed flat tympanograms (ie, days 14 through 16). Magnetic resonance imaging documented inflammation and fluid in 1 of the 11 nonparalyzed left ears and in all sham-inflated right ears. Lesser degrees of inflammation and effusion based on MRI evaluations were noted for the 3 air-inflated right ears that retained near-ambient pressures when compared with the right 3 ears that developed a flat tympanogram. The MRI measure of effusion quantity within the tympanum was decreased acutely after inflation, but was simultaneously increased in the adjacent airspaces of the temporal bone. Repeated air inflation prevented the development of otitis media with effusion in 50% of the ears with functional eustachian tube obstruction. Postinflation MRI documented the displacement of fluid by inflation from the tympanum to the mastoid and petrous air cells. Using standard clinical evaluations such as tympanometry and otoscopy, this fluid redistribution can cause a false diagnosis of improvement.

Repeated inflation does not prevent otitis media with effusion in a monkey model.

Investigate the efficacy of repeated middle ear inflation with an inert gas (argon) for preventing the development of middle ear effusion in monkeys with functional eustachian tube obstruction. Prospective controlled trial of daily middle ear inflation with five monkeys assigned to the inflation group and four to the control group. The right tensor veli palatini muscle of nine monkeys was paralyzed with botulinum toxin. Tympanometry was done before the procedure and then daily for 21 days. Presence and distribution of effusion were assessed before paralysis and on day 15 using magnetic resonance imaging (MRI). In five right ears inflation was done beginning at the first observation of negative middle ear pressure of < or =200 mm H2O and repeated on all days with pressures < or =-100 mm H2O. Four right ears served as uninflated controls. Right middle ear pressure decreased in all animals over the course of the study. Pressure returned to near-ambient levels immediately following the argon inflation but was decreased to control levels at the subsequent observation on the following day. MRI at day 15 documented effusion in all right ears with no quantifiable differences in amount or distribution between ears that were and were not inflated with argon. Repeated inflation with an inert gas does not prevent middle ear effusion in monkeys with functional eustachian tube obstruction.

Allergy induced eustachian tube and middle ear pathophysiology.

While these studies have provided evidence to support the contention that nasal allergy contributes to OME, they have not confirmed the hypothesis in its entirety. The provocative intranasal antigen or histamine challenges have induced eustachian tube obstruction but have not resulted in OME. Because we wanted to minimize the possible risk of creating middle ear pathology following a provocative intranasal challenge, the absence of a resultant OME was anticipated for two reasons: the relatively brief duration of eustachian tube obstruction after challenge and the use of adult study subjects. Following intranasal provocative challenge, the developed tubal obstruction persisted only for several hours to a few days. In monkeys OME does not develop until 1 to 4 weeks after creating a surgical functional eustachian tube obstruction. Thus, eustachian tube obstruction must be sustained for a week or more for OME to develop. Further, a number of studies have suggested that eustachian tube function improves with age and has been related to the fact that OME is more prevalent in younger children. If the younger child has some degree of functional eustachian tube obstruction, then the development of an antigen provoked, histamine mediated eustachian tube obstruction might be expected to have more severe and prolonged effects at a lesser antigen dosage. It is our hypothesis that allergy and other pathophysiologic events that release or generate mediators of inflammation in the nasopharynx play a role in the pathogenesis of middle ear diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of intranasal histamine challenge on eustachian tube function

Eustachian tube (ET) function was evaluated bilaterally by use of the inflation-deflation and forced-response test before and after nasal challenge with various doses of histamine in five adult and 10 infant rhesus monkeys ( Macaca mulatta). Of the 20 experiments conducted on the infant and juvenile monkeys, functional ET obstruction resulted in six ears after a dose of 0.5 mg of histamine, in 10 ears after a dose of 1 mg, and in four ears after a dose of 2 mg. In contrast, of the 10 experiments conducted on the adult monkeys, functional ET obstruction developed in two ears after a dose of 1 mg of histamine and in two ears after a dose of 4 mg. Six ears failed to respond at doses of 8 mg of histamine. The ET obstruction was characterized by increases in the values of the passive function parameters and an abolition of the ability to equilibrate applied middle ear pressures by muscular activity. ET obstruction was not observed in any ears after challenge with a saline control. The severity of the induced ET obstruction was lessened within 60 minutes after challenge. These data are similar to those reported for intranasal pollen challenges in sensitized rhesus monkeys and human volunteers and suggest that type I allergic reactions at the site of the nasopharyngeal mucosa disrupts the normal functioning of the ET by a mechanism potentially mediated by histamine release.

Effect of certain head and neck tumors and their management on the ventilatory function of the eustachian tube.

A prospective study was carried out which tested three hypotheses: 1) certain tumors of the head and neck that originate in sites other than the nasopharynx may cause middle ear effusion; 2) middle ear effusion is a predictable sequela of radical maxillectomy as well as total or partial resection of the soft palate; and 3) middle ear effusions that follow surgery to remove head and neck lesions are due to disturbances in palatal function, specifically to tensor veli palatini muscle dysfunction. Our results indicate that one fourth of all subjects had some evidence of middle ear abnormality prior to entering into treatment although they were asymptomatic. The treatment process influenced the function of the middle ear, as 79% of the subjects experienced middle ear-eustachian tube dysfunction following treatment, and 23% were found to have developed a perforation of the tympanic membrane or required myringotomy and tube insertion to relieve middle ear effusion. The results of these studies indicate that surgery that is adequate to remove cancer of the maxilla, tonsil, or palate in most cases interferes with the function of the tensor veli palatini muscle, resulting in functional eustachian tube obstruction. The need for attention to and the treatment of middle ear effusion in such patients is emphasized in light of other sensory deficits in this patient population.

Functional eustachian tube obstruction and otitis media in a primate model. A review.

In most infants and children with chronic otitis media with effusion, an inability to dilate the Eustachian tube actively has been documented. This functional tubal obstruction has been suggested to underlie the development of the disease. To test this possibility a variety of models using the Rhesus monkey were developed. The normal tubal dilatory system was impaired, resulting in sterile otitis media with effusion. The duration and nature of the disease was shown to be dependent on the severity and duration of the impairment in tubal function. These studies support the causative role of functional Eustachian tube obstruction in the development of otitis media with effusion and provide a series of models in which to study the etiology, pathogenesis, sequelae and complications as well as the treatment and preventions of the pathology in an animal species physiologically and anatomically similar to man.

Effect of surgical alterations of the tensor veli palatini muscle on eustachian tube function.

Previous studies in humans have indicated that functional obstruction of the eustachian tube (ET) is an important factor in the pathogenesis of otitis media with effusion (OME). This type of obstruction appears to be related to the structural properties of the tube, or to an inefficient active tubal opening mechanism, or both. In this study, functional ET obstruction was created in 22 rhesus monkeys (Macaca mulatta) by surgically altering the tensor veli palatini (TVP) muscle using three different procedures: 1) complete excision of the muscle; 2) transection of the superficial muscle bundle; or 3) transposition of the muscle tendon medial to the hamular process. Prior to surgery, weekly tympanometry, pneumatic otoscopy, and otomicroscpic examinations were performed for a period of at least six months to document middle ear (ME) status. A minimum of four ET function tests were performed on each animal using the inflation-deflation and forced-response tests. Following surgery, these tests and examinations were continued for periods of up to one year. Postoperatively, the animals in which the TVP had been excised developed a sterile ME effusion which proved to be a chronic condition which persisted throughout the follow-up period. Eustachian tube function tests showed a complete absence of any active tubal dilation by swallowing. Animals that had the muscle transected developed abnormal ME pressures , or effusions, or both, which returned to normal in some ears, but which were recurrent or chronic in others. Eustachian tube function tests in these animals showed an initial loss of active tubal function which gradually improved, but not to normal levels, presumably as a result of healing of the muscle. In cases in which the muscle was transposed the ME pathology and ET dysfunction were similar after the surgery, but improved within a short period of time. These data suggest that alteration of the TVP muscle can create functional obstruction of the ET. The severity of ET obstruction depends upon the surgical procedure undertaken. The results of postoperative ET function tests were similar to those recorded from children with recurrent and chronic OME.

Function of the Eustachian tube related to surgical management of acquired aural cholesteatoma in children.

A group of 12 children with acquired cholesteatoma had the ventilatory function of the Eustachian tube assessed by the inflation-deflation technique. All had varying degrees of functional rather than mechanical obstruction of the Eustachian tube. In these children, the pathogenesis of acquired cholesteatoma appeared to be the result of the following sequence of events: functional Eustachian tube obstruction, high negative middle ear pressure, atelectasis of the tympanic membrane-middle ear, a retraction pocket in either the posterosuperior or attic portion of the tympanic membrane, and adhesive otitis media. Tympanoplasty in these children was not successful. It is suggested that when the middle ear-mastoidectomy cavity is allowed to remain open, then the bony portion of the Eustachian tube should be surgically closed to prevent postoperative reflux of nasopharyngeal secretions.

Normal and abnormal middle ear ventilation.

Studies in infants and children have suggested a functional rather than mechanical obstruction of the Eustachian tube as a predisposing factor in middle ear effusions (MEE). To simulate this condition in the laboratory, an animal model was prepared using juvenile Rhesus monkeys. The tensor veli palatini muscle was transected or expunged posterior to the hamulus of the medial pterygoid lamina. Transection of the muscle resulted in negative middle ear pressure without effusion, whereas when the muscle was expunged, the animals developed a brief episode of negative middle ear pressure followed by a persistent MEE that was sterile for bacteria. An acute bacterial MEE developed following instillation of Streptococcus pneumoniae into the nasopharynx of animals that had had a previous unilateral transection of the muscle. The condition of the middle ear was documented by impedance measurements and presence of the effusion was verified by myringotomy. Animals were periodically examined and tested for Eustachian tube ventilatory function over a period of one year. Before surgical alteration of the tensor muscle. Eustachian tube function tests demonstrated normal ventilatory function, whereas, functional Eustachian tube obstruction patterns similar to studies in children who had MEE were found during the postoperative period. Only after the development of a reliable animal model can current and future methods of management of MEE be tested under controlled laboratory conditions. These data suggest that the Rhesus monkey appears to be an excellent model for the study of normal as well as abnormal tubal function.

Eustachian tube ventilatory function in relation to cleft palate.

The ventilatory function of the Eustachian tube was assessed in a group of infants and children with cleft palate, some of whom had received palatal repair. Those whose palates had been repaired were better able, in general, to equilibrate applied positive middle ear pressures than were those with open clefts. In many of the patients whose palates had been repaired, the results of Eustachian tube function studies were similar to those in normal subjects. Differences in Eustachian tube ventilatory function are assumed to be related to differences in tubal compliance. Excessive compliance probably results in, or exaggerates, functional Eustachian tube obstruction. Improvement in tubal function following palate repair is probably related to factors resulting in greater tubal stiffness.