--------------------------------------------------------------------------- TITLE: CHRONIC OTITIS MEDIA WITH EFFUSION SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: May 29, 1991 RESIDENT PHYSICIAN: Joseph J. Bradfield, MD FACULTY: Chester L. Strunk, MD DATABASE ADMINISTRATOR: Melinda McCracken, M.S. --------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." CHRONIC OTITIS MEDIA WITH EFFUSION I. Historical Perspective A. The presence of middle ear fluid has been recognized for centuries. 1. Politzer (1869) - described "otitis media catarrhalis". and recognized secretory and adhesive forms of the disease in his 1902 text. Middle ear fluid received little attention from then until the end of the second world war. 2. Hoople (1950) - described the clinical features of the disease and recommended early paracentesis for diagnosis. 3. Armstrong (1954) - advocated the polyethylene tube for ventilation and drainage. 4. Senturia (1958) - performed laboratory evaluations of ME effusions in animal models. II.Definition and Classification A. Otitis Media: a broad term used to refer to an inflammatory process of the middle ear. No reference is made either to the character of fluid present or the duration of the process. 1. Acute suppurative otitis media (acute purulent otitis media, acute otitis media) - The sudden onset and subsequent short duration of a clinically infected form of otitis media behind a reddened eardrum. One or more diagnostic signs are present - otalgia, otorrhea, fever, recent onset of irritability, anorexia, vomiting or diarrhea. 2. Otitis media with effusion (secretory or serous otitis media, nonsuppurative otitis media) - a clinically noninfectious form of fluid collection behind an intact TM. The duration may be classified as acute (less than 3 weeks), subacute (3 weeks to 3 months), or chronic (greater than 3 months). B. Chronic Suppurative Otitis Media( chronic otitis media)- usually refers to a chronic purulent discharge from the middle ear through a perforated tympanic membrane. C. Myringitis: refers to the inflammation of the tympanic membrane. It may or may not be associated with otitis externa or media. II. Anatomy and Physiology A. The eustachian tube ( ET ) is 17 to 18 mm at birth doubling in length to 35 mm. by adulthood. At birth the ET is horizontal but with growth it comes to lie at a 45 degree angle. It has 2 segments: 1. The medial fibrocartilaginous portion ( 24mm -2/3 of the total length): is closely applied to the base of the skull, and lies in a sulcus between the greater wing of the sphenoid and the petrous temporal bone. It usually extends about 3mm into the osseous portion. It has a crook shaped mediolateral and superior wall, and is completed laterally and inferiorly by a membrane which serves as an attachment for the fibers of the tensor veli palatini. 2. The lateral osseous portion: Lies entirely within the petrous temporal bone, and is directly contiguous with the anterior wall of the superior portion of the middle ear. Then lumen is roughly triangular, measuring 2 - 3mm vertically and 3 - 4mm along the horizontal base. B. Muscles associated with the eustachian tube include the tensor veli palatini, which is the sole active dilator of the eustachian tube; the levator veli palatini, related only by loose connective tissue; the salpingopharyngeuus and the tensor tympani. C. The mucous membrane of the ET and the middle ear is an extension and modification of the pseudostratified ciliated columnar epithelium of the upper respiratory tract. There are 3 structures found in the mucoperiosteum of the middle ear and mastoid: 1. Ciliated cells are prevalent near the ET opening and the hypotympanum. They decrease in number progressing back toward the mastoid. The cilia beat in metachronous waves and have small processes protruding from their tips that aid in transferring energy from the cilia to the mucous layer. 2. Submucosal glands are thought to secrete a periciliary fluid in which the majority of the length of each cilium is immersed. This combination is known as the mucociliary apparatus which has a number of important functions. It acts as a medium for removal of metabolites from, and a supply of nutrients to the ciliated cells. It also acts as a layer of low viscosity on which the mucous blanket can float, and acts as a spacer between the epithelium and the mucous blanket so only the tips of the cilia penetrate the mucous on the forward stroke, and may serve as a reservoir from which mucous hydration is maintained. The depth and viscosity of this blanket is critical for the proper functioning of the mucociliary apparatus. 3. Goblet cells produce a mucous of higher consistency. In the normal state these are present in low numbers in the middle ear. D. The ET has three physiologic functions: regulation of gas pressure within the middle ear, protection from nasopharyngeal secretions, and clearance of secretions from the middle ear into the nasopharynx. With normal ET functioning the intermittent opening due to contraction of the tensor veli palatini muscle during swallowing maintains ambient pressures in the middle ear. The amount of gas drawn into the tympanic cavity during the act of swallowing decreases as negative pressure within the middle ear increases. III. Pathophysiology A. Eustachian tube dysfunction is thought to be the primary cause of otitis media. Two major types of ET obstruction can lead to pathologic changes in the middle ear. 1. Functional obstruction results from collapse of the ET due to increased tubal compliance or an abnormal active opening mechanism. This type of obstruction is common in infants and younger children due to a decrease in the the amount and stiffness of the cartilage supporting the ET. Also, the tensor veli palatini muscle is less efficient before puberty due to age related differences in the skull base. 2.Mechanical obstruction may be either intrinsic or extrinsic. Intrinsic obstruction may result from abnormal geometry or intra- or extra-luminal factors which compromise the lumen. Most commonly this is due to inflammation from infection or allergy. Extrinsic obstruction may be due to extramural pressure from a supine position or from tubal compression related to a mass - for example the adenoids or tumor. B. With ET obstruction oxygen and nitrogen within the middle ear is resorbed leading to the development of a relative negative pressure. The rate of resorption of gases from the middle ear is reported to be about 1cc/24 hours. This negative pressure leads to transudation of fluid and resultant edema of the muco-periosteum. This transudate occurs as a passive transfer of serous fluid from the subepithelial vessels. C. Infection, persistent effusion and epithelial damage promote the release of a number of potent inflammatory mediators. Together with the presence of bacterial toxins and enzymes and an increase in the partial pressure of CO2, these mediators stimulate metaplasia of the ET and middle ear epithelium to a more secretory type characteristic of the lower respiratory tract. There is an increase in mucus producing goblet cells and enlargement of the subepithelial glands with a resultant increase in production of mucous to protect the irritated epithelium. D. Abnormalities of the mucociliary blanket result. As the blanket becomes too thick cilia do not penetrate the mucous and their effectiveness is reduced. Production of tenacious mucous may cause adherence of the mucous blanket, anchoring it in place, and preventing the secretion of a less viscous mucous. E. In extreme cases, an abnormally patulous tube may be open even at rest, lesser degrees of abnormal patency may result in a semi- patulous ET that is closed at rest but has a lower opening resistance than a normal ET. This can result in failure to protect the middle ear from nasopharyngeal secretions and can result in "reflux otitis media". American Indians and Eskimos have been found to have abnormally patent ET. F. Various other factors have been associated with the development of otitis media with effusion: 1.Viral infection is frequently associated with otitis media. Researchers have demonstrated a correlation between isolation of viruses from the upper respiratory tract and the clinical diagnosis of otitis media. OM was increased in the 14 days following upper respiratory isolation of RSV, adenovirus, influenzae a and b, mumps and enterovirus.RSV has further been shown to induce a state of IgE-mediated hypersensitivity in the nasopharynx. Bacterial infection is felt to be predominantly secondary to viral infection. Viruses are infrequently cultured from the middle ear in otitis media. 2. Adenoids are rarely large enough themselves to cause mechanical obstruction but the obstruction of lymphatics draining the middle ear and ET may be a factor of greater importance. Chronic adenoiditis may provide a focus of pathogenic bacteria adjacent to the tubal orifice. Gates found no correlation between the size of the adenoid pad and resolution of COME after adenoidectomy - therefore the main benefit of adenoidectomy may be the reduction in the bacterial flora of the nasopharynx. 3. Allergy: Multiple studies have tried with varying success to prove or disprove an allergic effect on the ME mucosa and eustachian tube. Friedman showed that a provocative intranasal pollen application produced allergic rhinitis followed by ET obstruction, and that allergic reactions in the nose and nasopharynx inhibit even transient dilatations of the ET tube during swallowing. Bernstien found that in 15% of children with proven allergy, there was evidence of the middle ear as a target organ. The exact method by which allergy affects ET function is elusive, but three different immunologic mechanisms may play a role in the pathogenesis of COME: a. IgE mediated hypersensitivity - Bernstein et al demonstrated the independent local production of nasal and middle ear IgE. b. Immune complexes - studies suggest these do occur in the middle ear but are felt to represent normal immuno-elimination of bacteria and viruses rather than being pathologic for the middle ear mucosa. c. Delayed hypersensitivity - macrophages and lymphocytes predominate in chronic middle ear effusions. Perivascular infiltration of mononuclear cells is classic for delayed hypersensitivity and is often seen in COME. 4. Sinusitis - chronic sinus infection often times parallels similar process within the middle ear. 5. Cleft palate is almost universally associated with COME in children with unrepaired clefts, probably due to functional obstruction of the ET. Submucous clefts appear to have the same risk for COME, and there is a high incidence of OM in children with bifid uvulae. Studies have demonstrated that the ETs of patients with cleft palates constrict instead of dilating during swallowing. 6. Tumors - a unilateral middle ear effusion in an adult is tumor until proven otherwise. IV. Epidemiology and Screening A. Otitis media results in approximately 30 million office visits per year, and more than $2 billion is spent annually in the U.S. for care of OM. Myringotomy with tube insertion is the most commonly performed procedure requiring general anesthesia. Tonsillectomy and adenoidectomy is the most commonly performed major surgical procedure in children. B. The highest attack rates for acute otitis media occur in children under two years of age. Teele demonstrated that in one patient population, over 70% of the children had at least one episode of OM by age three. Rates are higher in the winter months, in boys, in children placed in day care centers, and in children who come from low socioeconomic class. Eskimos and Indians are affected more frequently than Caucasians or Blacks. Premature infants, those born to smoking mothers, and bottle fed infants also have a higher risk for otitis media. C. Three weeks after treatment of acute otitis media 75-90% of children will have a middle ear effusion. By three months all but 10% will be effusion free. D. Tos has estimated the prevalence of Type B tympanograms - usually associated with COME to be from 10 - 20% in a preschool population studied. After age 6, age related improvements are seen. Spontaneous improvement in tympanograms was seen in better than half the patients over a three month period. E. In the populations studied by Tos up to 80 - 90% of preschool children had one episode of secretory otitis media, characterized by the presence of a Type B or C2 tympanogram. The conditions took the following courses: 1. In 15% of the cases a short lasting (1 -3 month) single episode occurred. 2. Short lasting recurrent cases usually associated with upper respiratory infections occurred in 25% of the population. 3. Single prolonged (3 to 9 months) cases occured in 15% of the population and were associated with moderate eardrum sequelae. 4. Prolonged recurrent episode occured in 15% of the ears and resulted in marked changes in the TM. 5. Very prolonged episodes of 1 - 4 years duration occurred in 10% of the ears. These were associated with marked changes in the ME mucosa and TM. F. For children under two years of age otoscopic exam combined with tympanometry is highly accurate for detecting COME. The Third Postsymposium Research Conference recommends combining tympanometry with pure tone screening. V. Bacteriology A. Bluestone reports that bacteria were cultured from over 80% of middle ear effusions in acute otitis media. S. pneumonia, H. influenza and B. catarrhalis predominate. B. Cultures from COME ears were positive in over 2/3 cases - with the same organisms predominating. Some investigators feel this indicates that an inadequately treated acute otitis media is responsible for the development of COME. VI. Sequelae A. Attic retractions in childhood are primarily associated with negative pressure within the middle ear, and may or may not be associated with pars tensa retractions. Four types of attic retractions are identified, progressing from slight, harmless retractions to those with bony resorption of the annulus and adherence to the malleus. As long as the retraction remains self cleaning, the condition may be considered stable. However, if the migration of extruded keratin debris is disrupted, accumulation of keratin may occur resulting in a precholesteatoma and cholesteatoma. If an attic retraction requires frequent cleaning and shows a tendency toward precholesteatoma surgery may be indicated. B. Pars Tensa sequela include atrophy, tympanosclerosis, retraction and adhesion, any of which may occur concomittantly, as well as perforation. Most frequently atrophy and tympanosclerosis or atrophy and retraction are seen together. 1. Atrophy denotes a thin, pellucid membrane and is characterized histologically by a thin lamina propria and decreased elastic fibers. The atrophy may be diffuse or localized. Diffuse atrophy with retraction (atelectasis) may result in the TM becoming adherent to infected ME mucosa (adhesive otitis). Although negative pressure within the ME space may original result in atelectasis, it may no longer be present upon presentation. Retraction of the posterior - superior aspect of the pars tensa is more frequently associated with serious sequela. Posterior superior retraction may result in myringostapediopexy and bony resorption of the ossicles. The presence of inflammatory mediators within the middle ear is thought to be a factor in ossicular erosion and permanent middle ear mucosal changes. Adhesive otitis is irreversible and may progress to cholesteatoma. Following insertion of a PE tube, an area of retraction should return to a more neutral position. If this does not occur, then adhesive otitis is present. Tympanoplasty is a reasonable method of treatment at this point to prevent progression. 2. Perforations may result in areas of atrophic tympanic membrane from local trauma that would be insignificant in normal TMs, and due to compromised vascular supply these perforations are at greater risk to not heal spontaneously. 3. Tympanosclerosis is defined as a hyalin degeneration of the fibrous and elastic fibers of the lamina propria, resulting in yellowish plaques in the TM and ME, and is considered an irreversible nonspecific end result of chronic infection or inflammation. C. Bony resorption occurs in secretory otitis media as well as in cholesteatoma and chronic suppurative OM. Bone resorption is commonly found in: 1. The bony annulus in type III and IV attic retractions. 2. Spontaneous atticotomy or cavity formation when infection occurs within a retraction. 3. Resorption of the long process of the incus (most common), progressing to myringoincudopexy and subsequently to myringostapediopexy. 4. Partial resorption of the stapes superstructure. 5. Partial resorption of the malleus handle in the case of pars tensa atelectasis and retraction. D. Decreased mastoid cellularity and pneumatization has been well documented in chronic otitis. There is, however some controversy as to whether this is a cause or an effect. Recent studies are strongly supportive of the theory that this hypocellularity is the sequela of chronic infection and inflammation. Sade claims that the better pneumatized the mastoid, the better the prognosis, and that the disease course is more protracted in those with poor pneumatiztion. E. Sensorineural hearing loss has also been documented as a long term complication of chronic otitis media with effusion. The mechanism may be associated with lack of oxygen supply to the inner ear from the ME. Other studies have documented changes in round window permeability and cochlear changes in expirementally induced otitis media. However, it remains controversial as to what part the presence of middle ear effusion plays in the development of permanent hearing loss. F. Developmental delay has been demonstrated in large numbers of studies which suggest a causal relationship between early hearing loss and developmental delay. However existing evidence also suggests that once hearing has recovered in young children that developmental impairment tends to disappear. Therefore there is no convincing evidence that adverse development of a lasting nature can result from COME in the first few years of life provided that normal hearing is eventually attained. VII. Management A. The clinician must decide whether or not to treat or watch a patient with COME based on the knowledge that the complications and sequelae associated with this condition are not fully known. Further, considerable data exists indicating that the majority of these patients resolve spontaneously. In addition to hearing loss, Bluestone recommends considering the following factors when formulating a treatment plan for a COME patient: 1. Young infants are unable to communicate about their disease and may have suppuration. 2. Concurrent permanent conductive or sensorineural hearing loss. 3. The presence of an associated acute purulent upper respiratory tract condition. 4. Alterations of the tympanic membrane such as severe atelectasis and attic retraction pockets 5. Presence of vertigo or tinnitus. 6. The presence of middle ear changes. 7. Fears and frustrations of the parents and/or patient. 8. Costs and inconvenience of the form of treatment to that particular patient. 9. Whether or not the patient is in school. B. The goals of treatment should be : 1. To normalize hearing loss. 2. To prevent recurrent episodes of acute OM in those patients in whom secretory OM is part of a syndrome of recurrent OM. 3. To prevent long term complications. C. Medical therapy - of the many forms of medical treatment none has been shown to be effective in acceptable clinical trials. l. Oral decongestants/antihistamines have been shown by Cantekin to be ineffective in infants and children with acute, subaacute and chronic OME. They may be effective in adolescents or in adults, or in patients in whom there is evidence of otolaryngic allergy. 2. Mucolytic agents - clinical trials with urea, bromhexine, and thiol compounds have been conducted under the theory of degrading the tenacious secretions to produce a decrease in viscoelasticity. We are currently evaluating the use of guiafenesin in children with COME. 3. Antiinflammatory compounds - trials have been performed with these drugs under the hypothesis of neutralizing the inflammatory mediators of the condition. The efficacy of oral steroids has been suggested by some studies. Giebink et al evaluated the use TMP - SMX as compared to prednisone or ibuprofen for persistent ME effusion. Although the TMP-SMX and prednisone treated groups initially fared better, there were no long term statistically significant differences. Podoshin treated 136 children in a randomized, double blinded study and demonstrated a significantly improved response to amoxicillin and prednisone versus amoxicillin alone. The treatment most benefitted children 4 - 10 without oversized adenoids. However, many clinicians feel the risks of steroids may outweigh their benefits in the treatment of this condition. 4. Immunotherapy - there are several anecdotal reports of successful treatment of COME with allergy desensitization. However the majority of these reports lack a controlled study. Hurst treated 20 patients with refractory COME with immunotherapy. All improved their symptoms, although 35% relapsed due to poor compliance. Allergy therapy should be considered in patients with a strong allergic history. 5. Antibiotics - of all the treatments advocated, a trial of antibiotics appears to be most appropriate, especially in child that has not been previously so treated, to eradicate any bacteria that may be an etiologic factor. Mandel has demonstrated the efficacy of amoxicillin in some children with OME. Amoxicillin - clavulanate has also been shown to be an effective treatment. Gates has recommended an additional period of antibiotics and observation in a child referred for surgical therapy - he noted in a study of 2224 ears, 63% cleared within two months on this therapy. He noted better results in older children and in those with peaked tympanograms. D. Surgical treatment l. ET inflation - this has been long practiced using either the Politzer method or employing the Valsalva maneuver. Sade has demonstrated that the improvement gained from politzerization lasts only about 40 - 60 minutes, and does not change the course of the disease. In a recent controlled study in children with refractory OME, however, Chan and Bluestone demonstrated autoinsufflation to be of no clinical value. Nevertheless, this treatment may be of benefit in adults and in the treatment of serous effusions of short duration. 2. Adenoidectomy - adenoidectomy has long been advocated for the treatment of otitis media based upon the theories that enlarged adenoids could cause mechanical obstruction of the ET; that adenoidectomy would improve the passage of air through the ET; and that adenoidectomy reduces the incidence of recurrence of OM. Multiple studies have been undertaken to prove or disprove these hypotheses. Most of the studies suffer from one or more shortcomings, and the controversy continues. In his extensive review, Sade examined these studies and concluded that most of the underlying rationale for adenoidectomy in the treatment of COME was incorrect. However there is evidence from studies by Gates, Maw, and Paradise that adenoidectomy may reduce the need for multiple sets of tubes in a certain subpopulation of patients, decreasing their relapse rates in half. 3. Myringotomy with or without tube insertion - most authors advocate myringotomy and tube placement if the child is to undergo general anesthesia. Bluestone recommends myringotomy alone if the child is old enough, followed by M&T for recurrences. BM&T relieves the immediate problem of fluid, negative pressure, and hearing loss but its efficacy in permanent resolution of the underlying disease process remains unproven. Most studies report 75 - 80% of patients require only one set of tubes. a. Luxford and Sheehy reported on 1568 ears. They report the following complications: - Otorrhea - this occurred in 19% of patients but necessitated tube removal in only 9 patients. In comparing this to a 5% rate of otorrhea which occured in their patients who underwent BM&T for symptoms of a patulous ET they concluded that otorrhea following BM&T for COME is more related to the disease process than to the presence of the tube. Tos recommends that if otorrhea has not ceased after 1 - 2 months of antibiotics and local treatment, then the tube should be removed. If drainage continues for an additional 2 - 3 months, cortical mastoidectomy may be needed. - Persistent perforation - 4% of patients had perforations, the majority of which had undergone multiple intubations. Other studies have reported rates varying from 0.5 - 2%. Perforations caused by tubes should probably not be closed for a couple of years - until the ME mucosa and ET function have improved. b. Weigel evaluated 4 different types of tympanostomy tubes in 75 patients. - The T-tube was associated with a longer period of retention past two years, plugging and otorrhea, and was the only tube associated with residual perforations requiring T-plasty. - The Reuter Bobbin was associated with a higher rate of plugging. c. Other studies have demonstrated an increase in the incidence of tympanosclerosis in ears receiving PE tubes. However, there does not appear to be any significant long term effect on hearing (3 - 8 years after BM&T). 4. Exploratory tympanotomy and mastoidectomy - a small percentage of patients may have persistent otorrhea despite the removal of the tube, or may be found to have black fluid at the time of myringotomy. Exploration in these patients is reasonable to rule out a cholesterol granuloma or other pathology. In secretory OM however, this procedure should be reserved for those in whom mastoid osteitis or cholesteatoma is suspected. Further, exploration and tympanoplasty may be indicated in patients with non-stable retraction disease, adhesive otitis, or precholesteatoma, as described above. ---------------------------------------------------------------------------- Bibliography 1. Gates GA, Holt GR: Medical Treatment of Chronic Otitis Media with Effusion. Otolaryngol Head Neck Surg 1986 Mar:94:350-4. 2. Recent Advances in Otitis Media with Effusion. Report of research conference, May 20-21, 1983. Ann Otol Rhinol Laryngol ( suppl ) 1985 Jan-Feb: 116:1-32. 3. Maw AR, Speller DC: Are the Tonsils and Adenoids a Reservoir of Infection in Otitis Media with Effusion? Clin Otolaryngol 1985 Oct; 10:265-9. 4. Maw AR: FActors Affecting Adenoidectomy for Otitis Media with Effusion. J R Soc Med 1985 dec 78:1014-8. 5. Bernstein JM: Recent Advances in Otitis Media with Effusion. Ann Allergy 1985 Oct 55: 544-51. 6. Bluestone CD: Antimicrobial Therapy for Otitis Media with Effusion. Ped Ann 1984 13: 405-410. 7. Paradise JL: Inadequate Resolution of Acute Otitis Media Following Antimicrobial Therapy. Ped Ann 1984 13: 382-390. 8. Smyth GDL: Management of Otitis Media with Effusion: A Review. Am J Otol 1984 5: 344-348. 9. Paradise JL: Otitis Media During Early Life: How Hazardous to Developement? Pediatrics 1981 68: 869-873. 10. Luxford WM, Sheehy JL: Myringotomy and Ventilation Tubes: A Report of 1568 Ears. Laryngoscope 1982 92: 1293-1297. 11. Gottschalk GH: Tympanostomy Tubes: To Be or Not To Be? Am J Otol 1984 5: 248-250. 12. Armstrong BW: Ventilating Tubes Are the Treatment of Choice For Chronic Nonsuppurative Otitis Media. Am J Otol 1984 5: 250-251. 13. Brown DT, et al: Drugs Affecting Clearance of Middle Ear Secretions: A Perspective for the Management of Otitis Media with Effusion. Ann Otol Rhinol Laryngol 1985 116: 3-13. 14. Bluestone CD, Klein J: Otitis Media in Infants and Children; W.B. Sanders Company; 1988. 15. Gates GA, et al: Effectiveness of Adenoidectomy and Tympanostomy Tubes in the Treatment of Chronic Otitis Media with Effusion. NEJM 1987 Dec: 1444-1451. 16. Gates, GA et al: Effect of Adenoidectomy on Children with Chronic Otitis Media With Effusion. Laryngoscope 1988 98: 58- 63. 17. Gates GA: Post Tympanostomy Tube Otorrhea. Laryngoscope 1986 96: 630-634. 18. Divan, et al: Hydrolase Activity in Middle Ear Effusions. Archives Otol - Head and Neck Surgery 1988 Jan 114: 52-55. 19. Gates GA, et al: Delayed Onset Post-Tympanostomy Tube Otorrhea. Otol - Head and Neck Surgery 1988 Feb 98: 111-115. 20. Chan K, et al: A Comparative Study of Amoxicillin Clavulanate and Amoxicillin. Archives Otol - Head and Neck Surgery 1988 Feb 114: 137-141. 21. Chan KH, and Bluestone CD: Lack of Efficacy of Middle Ear Inflation: Treatment of Otitis Media With Effusion in Children. Otol - Head and Neck Surgery 1989 Apr 100: 317-323. 22. Thomsen J, et al: Antibiotic Tratment of Children with Secretory Otitis Media. Archives Otol - Head and Neck Surgery 1989 Apr 115: 447-451. 23. Hurst DS: Allergy Management of Serous Otitis Media. Otol - Head and Neck Surgery 1990 June 102: 664-669. 24. Podoshin L, et al: The Efficacy of Oral Steroids in the Treatment of Persistent Otitis Media with Effusion. Archives Otol - Head and Neck Surgery 1990 Dec 116: 1404-1406. 25. Paden EP, et al: Recovery from OME Related Phonologic Delay Following Tube Placement. Jour Speech and Hearing 1989 Feb 54: 94-100. 26. Bluestone CD: Otitis Media And Related Conditions. In English, Otolaryngology. Philadelphia: JB Lippincot Company 1990. 27. Tos M: Chronic Otitis Media and Cholesteatoma. In English, Otolaryngology. Philadelphia: JB Lippincot Company 1990. 28. Weigel MT, et al: A prospective Randomized Study of Fpur Commonly Used Tympanostomy Tubes. Laryngoscope 1989 Mar 99: 252-256. 29. Bluestone CD: Modern Management of Otitis Media. Pediatric Clinics Of North America 1989 Dec 36: 1371-1387. 30. Sade J, and Luntz M: Adenoidectomy in Otitis Media. Ann Otol Rhinol Laryngol 1991 100: 226-231. 31. Giebink GS, et al: A controlled Trial Comparing Three Treatments for Chronic Otitis Media with Effusion. Pediatr Infec Dis J 1990 Jan 9: 033-040. 32. Sade J, Luntz M, Pitashny R: Diagnosis and Treatment of Secretory Otitis Media. Otolaryngologic Clinics of North America 1989 Feb 22: 1-14. 33. Chinh TL, et al: Evaluation of Ventilating Tubes and Myringotomy in the Treatment of Persistent Otitis Media. Pediatr Infec Dis J 1991 Jan 10: 2-11. 34. Austin DF: Adenoidectomy for Secretory Otitis Media. Archives Otol - Head and Neck Surgery 1989 Aug 115: 936-939. 35. Tos M: Ventilating Tubes for Middle Ear Effusions. In English, Otolaryngology. Philadelphia, JB Lippincott Company, 1990. 36. Paparella and Shumrick: Otolaryngology. Philadelphia, WB Saunders Company, 1980. -----------------------------------END------------------------------------------ TEST QUESTIONS - The following test questions are intended to provide proof to accrediting agencies that you have read and understood the entire Grand Rounds element. Your answers should be based on the text of the Grand Rounds element. Answers should be sent by e-mail addressed to fbquinn@utmb.edu. Answers can be sent by U.S Postal Service mail, using a plain sheet of paper on which the Grand Rounds element and the subscriber are fully identified. Correct answers will be transmitted to the subscriber via e-mail. Comments and alternative points of view should be expressed at the end of the list of the subscriber's answers. The University of Texas Medical Branch (UTMB) is accredited by the Accreditation Council For Continuing Medical Education (ACCME) to sponsor continuing medical education for physicians. UTME designates this continuing medical education activity for 1 credit hour in Category 1 of the Physicians's Recognition Award of the American Medical Association. 1. All of the following are signs of acute suppurative otitis media except a. ear pain b. headache c. fever d. otorrhea 2. The tensor veli palatini musscle a. causes posterior movement of the pinna b. regulates movement of the ossicular chain c. maintains ambient pressure in the middle ear d. is the sole constrictor of the eustachian tube 3. The eustachean tube functions include a. providing a channel for CN VII into the middle ear b. regulation of gas pressure within the middle ear c. protection of the middle ear from nasopharyngeal secretions d. clearance of secretions from the middle ear into the pharynx 4. The primary cause of otitis media is thought to be a. eustachean tube dysfunction b. otitis externa with eardrum perforation c. barotrauma d poor compliance of the tymanic membrane 5. With eustachean tube obstruction, oxygen and nitrogen within the middle ear are reabsorbed, leading to the development of a. localized metabolic acidosis b. disordered equilibrium c. negative pressure and edema b. positive pressure and edema 6. Eustachean tubes having an abnormally low opening resistance can lead to a. serous otitis media b. bullous myringitis c. Meniere's disease d. reflux otitis media 7. All of the following factors are know to contribute to the development of otitis media with effusion except a. viral infection b. cerebral palshy c. sinus infections d. unrepaired cleft palate 8. What percentage of children will have middle ear effusion as long as three weeks after successfully treated acute otitis media? a. 5-10% b. 20-35% c. about 50% d. 75-90% 9. Treatment goals for chronic otitis media with effusion should include all of the following except a. normal hearing b. prevention of recurrent acute otitis media c. reduced incidence of tinnitus and vertigo d. prevention of the complications of inadequately treated otitis media 10. Which class of drugs provides the most generally effective treatment of chronic otitis media with effusion a. antibiotics b. decongestants/antihistamines c. mucolytics d. anti-inflammatory agents 11. Which of the following statements is false? a. Eustachean tube autoinflation may help resolve middle ear effusion in adult patients b. Enlarged adenoid has not been conclusively proven to cause obstruction of the eustachean tube c. Myringotomy with tube insertion through the eardrum relieves the immediate problems of fluid accumulation, negative pressure, and conductive hearing loss d. Tympanoplasty is indicated in all cases of tympanic membrane perforation in order to prevent future development of chronic otitis media 12. Potential complications of tympanostomy tube insertion include all of the following except a. tympanosclerosis b. persistent eardrum perforation c. persistent otorrhea d. chronic mastoiditis In order for the sponsors of this CME activity to monitor its usefulness and appropriateness to subscribers, we ask that your supply answers to the following questions concerning the accompanying Grand Rounds Online CME segment: 1. Was the presentation organized in an acceptable manner? yes no opinion no 2. Was the material adequate to your continuing education needs with respect to content? yes no opinion no 3. Was the material appropriate to your clinical practice needs? yes no opinion no 4. Did you feel that the discussants' remarks were responsive to the issues presented in the body of the Grand Rounds segment? yes no opinion no 5. Do you consider the presentation to be timely with regard to current information available in both the lay press and the professional literature? yes no opinion no 6. Are the questions submitted with the Grand Rounds element meaningful in that they stimulate thought and perhaps further inquiry? yes no opinion no 7. Is the method of submitting the subscriber's answers to these questions expeditious and convenient? yes no opinion no 8. Would you recommend this method of completing the general requirment for Continuing Education Activity to your colleagues? yes no opinion no 10. How much money (U.S. dollars) would you be willing to pay for each award of 10 or more CME Category I credits earrned through this type of online CME activity? $100 $50 $25 $12.50 $6.25 $3.00 $1.50 $0.75 $0.35 $0.15 Please submit any comments, criticisms and suggestions which you may have in the space below. They will be given thoughtful consideration, especially if they are favorable comments, gentle criticisms, or constructive suggestions. 8-) /s/ The Editor. ================================================================== Francis B. Quinn, Jr., M.D. University of Texas Medical Branch Dept. of Otolaryngology Galveston, TX 77555-0521 Internet addresses: 409-772-2706, 772-2701 fbquinn@UTMB.edu 409-772-1715 FAX fbquinn@phil.utmb.edu ==================================================================