TYMPANOMETRY IN CHILDREN WITH TREATED ACUTE OTITIS MEDIA

529

Reports from Africa have suggested, but not proven, that male heterosexuals with evidence of exposure to the AIDS retrovirus contracted it from antibody-positive prostitutes.7,8 Since the AIDS virus is known to be transmitted to females via contact with male carriers of the virus,12,13these prostitutes could have been infected by the virus-positive men. Moreover, as of December, 1985; only 28 men with AIDS in the United States appeared to have been infected with the AIDS virus through contact with high-risk women (Centers for Disease Control, personal communication). This number represents less than 01% of all AIDS cases in the United States. Our results however support the notion that the virus could have infected these 28 males through normal vaginal intercourse. Our finding of low amounts of replicating ARV is also consistent with the epidemiological evidence that this route of transmission is rare; nevertheless, conditions of the vagina in a state of low arousal do not necessarily reflect the situation during intercourse. The one sample obtained postorgasm did reveal virus although not at levels any higher than other positive samples. The virus might be passed more easily by women who have concurrent venereal infections with copious inflammatory secretions in the vaginal canal containing many virus-infected lymphocytes. Moreover, since it appears that ARV needs access to the bloodstream, the clinical status of the penile and urethral epithelia of the male partner may contribute importantly to his susceptibility to AIDS virus infection. The recovery of ARV in vaginal secretions from antibodypositive women emphasises the need for safe-sex guidelines for virus-infected men and women, including use of prophylactic sheaths by high-risk groups. 14 These studies were conducted as part of a research programme of the Association of Women’s AIDS Research and Education (AWARE), AIDS Activities Unit, San Francisco General Hospital, and the San Francisco Women’s Cohort Study. The research was supported by USPHS Grant 34980 from the NCI and grants from the California State Universitywide Task Force on AIDS. We thank Dr John Mills for conducting the herpes simplex virus and cytomegalovirus studies on the vaginal and cervical secretions. We appreciate the help of Ms Denise Hardy with the serological tests and Ms Teresa Kendrick with the reverse transcriptase assays. We thank Ms Linda Marquis, Ms Lauren Poole, and Ms Bernadette Cracchiolo for their assistance in the evaluation and counselling of the study participants.

Correspondence should be addressed to J. A. L., Department of Medicine, Cancer Research Institute, University of California, San Francisco, CA 94143, USA.

TYMPANOMETRY IN CHILDREN WITH TREATED ACUTE OTITIS MEDIA MICHAEL T. K. WHEELER Fairweather Health

Centre, Cardiff CF5 3JT

Tympanometry was used to identify middleear changes in 154 children with otitis media during and after treatment in general practice. In two hundred and nineteen episodes, 242 infected and 196 non-

Summary

infected ears were examined. The results suggest that chronic serous otitis media or "glue ear" is not a consequence of acute otitis media; that persistence of middle-ear effusion is unlikely to predispose to recurrent acute otitis media; and that in unilateral otitis media abnormalities are often present in both ears.

Introduction THE main abnormalities in acute otitis media are inflammation of the mucosa lining the middle ear, the ossicular chain, and the deep surface of the tympanic membrane; an effusion; and reduced air pressure with retraction of the tympanic membrane.’,’ The duration of pathological changes after resolution of the acute infection is uncertain.3These changes have been implicated in the causation of deafness, and long-lasting effusion is thought to be a causal factor in chronic serous otitis media or glue ear.4-6 In addition, persistent effusion could predispose to the recurrence of acute otitis media.6,7 Black8 has suggested that the epidemic of surgically treated glue ear is due to unnecessary surgical treatment of effusions that would have resolved spontaneously. Methods for study of the sequelae of acute otitis media include the interpretation of the state of the tympanic membrane, in which observer variation is wide, and the presence of middle ear pathology as identified by deafness, for which there is no universal definition.9-"Tympanometry has been used little in the study of acute otitis media, although this technique gives information on several elements in the condition-the patency of the eustachian tube; the state of the tympanic membrane and ossicular chain; and the presence of fluid in the middle ear. 13 This study was undertaken to identify, by tympanometry, the middle-ear changes that arose during and after the acute infection in children.

REFERENCES

2

3 4

5

6 7

8.

9.

F, Chermann JC, Rey F, et al. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome. Science 1983; 220: 868-71. Gallo R, Salahaddin SZ, Popovic M, et al. Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk of AIDS. Science 1984; 224: 500-03. Levy JA, Hoffman A, Kramer S, et al Isolation of lymphocytopathic retroviruses from San Francisco patients with AIDS. Science 1984; 225: 840-42. Levy JA, Kaminsky LS, Morrow WJW, et al. Infection by the retroviruses associated with the acquired immunodeficiency syndrome. Ann Intern Med 1985; 103: 694-99. Levy JA, Hollander H, Shimabukuro J, Mills J, Kaminsky L. Isolation of AIDS associated retroviruses from cerebrospinal fluid and brain of patients with neurological symptoms. Lancet 1985; ii. 586-88. Centers for Disease Control. Heterosexual transmission of human T-lymphotropic virus type III/lymphadenopathy associated virus. MMWR 1985; 34: 561-63. Van de Perre P, Carael M, Robert-Guroff M, et al Female prostitutes: a risk group for infection with human T-cell lymphotropic virus type III Lancet 1985; ii: 524-26. Clumeck N, Robert-Guroff M, Van de Perre P, et al. Seroepidemiological studies of HTLV-III antibody prevalence among selected groups of heterosexual Africans. JAMA 1985; 254: 2599-602. Kaminsky LS, McHugh T, Stites D, et al High prevalence of antibodies to AIDSassociated retroviruses (ARV) in acquired immune deficiency syndrome and related conditions and not in other disease states. Proc Natl Acad Sci USA 1985; 82: 5535-39.

Methods

1. Barré-Sinoussi

The study was undertaken in a mainly urban general practice of 8500 patients, of whom 1200 persons were under twelve years of age. Included were 154 children under the age of twelve years with episodes of acute otitis media (between Nov 1, 1978 and Oct 31, 1980) in whom it was possible to perform tympanometry. Acute otitis media was defined as earache and an acutely inflamed tympanic membrane, of which at least two-thirds had to be

10.

Levy JA, Shimabukuro Recovery of AIDS-associated retroviruses from patients with AIDS, related conditions and clinically healthy individuals. J Infect Dis 1985; 152: 734-38.

11. Hoffman AD, Banapour B, Levy JA. Characterisation of the AIDS-associated retrovirus reverse transcriptase and optimal conditions for its detection in virions.

Virology 1985; 147: 326-35. JK, Kitchen LW, Prince HE, et al. Antibody to human T-lymphotropic virus type III in wives of hemophiliacs. Ann Intern Med 1985; 102: 623-26. Harris C, Small CB, Klein RS, et al. Immunodeficiency in female sexual partners of men with the acquired immunodeficiency syndrome. N Engl J Med 1983; 308:

12. Kreiss

13.

1181-84. 14. Conant M, Hardy

D, Sernatinger J, Spicer D, Levy JA. Condoms prevent transmission retrovirus. JAMA (in press)

of the AIDS-associated

530 involved.

Deafness

and

aural

discharge

were

regarded

as

confirmatory signs when present, but were not essential for diagnosis. In each episode, infected and non-infected ears were examined by tympanometry at presentation. Each patient was provided with a

day course of ampicillin (125 mg four times a day for those four years old, 75 mg four times daily for those under four). Tympanometry was repeated at the first, third, and seventh week after presentation and thereafter every four weeks until the findings had returned to normal. Tympanometry was performed with a Peters AP 61c portable electro acoustic impedance bridge, the normal range of middle-ear pressure being taken as + 50 to -100 mm H20. The measurement of compliance is the least accurate of the tympanometric measurements13,14 and its normal range is considerable (0-3-1’ 5 ml), but a low compliance has been associated with otosclerosis and a high compliance with dislocation of the ossicular chain and a flaccid tympanic membrane.13-15 To measure the effect of the resolving inflammatory process on the tympanic membrane and on the mucosa of the ossicular chain, compliance was judged normal when it was more than half the mean compliance of both ears when they had returned to normal The interpretation of tympanograms was based on the Jerger

Type III,

membrane and the

and

over

see

figure. Tympanograms

were

designated

as

follows:

Type I, effusion; Type II, reduced

pressure without effusion, suggesting that pressure reduction is secondary to eustacian tube

dysfunction;

compliance without effusion, suggesting an inflammatory change involving the tympanic mucosa

of the ossicular chain;

Type IV, compliance and pressure reduction without effusion, suggesting inflammation of the tympanic membrane

seven

classification,16

reduced

Typ (This

mucosa

pressure; e V, normal. method is not

of the ossicular chain and reduced air

perfect:

when

a

type I tympanogram

is

recorded, an effusion is not invariably present; and types II, III and IV are recorded where effusions are present.

occasionally 17,19)

When the tympanograms in both ears were normal and of similar shape, normality was confirmed in each episode by testing both ears means of a 2000 Hz sound at for contralateral stapedial reflexes 100 dB above the hearing threshold. 9 If the stapedial reflex was not present in both ears, tympanometry was repeated at intervals until the reflexes were present.

bty

Results

Tympanometry was tolerated well by most children and caused no great discomfort, even during the acute infection. The main difficulty was in getting younger children to sit still for the test. 23 episodes of bilateral and 196 episodes of unilateral acute otitis media were observed. So the middle ear was assessed in 242 infected and 196 non-infected ears. Most of the infected ears showed type I tympanograms (effusions) (table I). Middle-ear changes were also recorded in about two-thirds of non-infected ears. During acute infection reduced compliance (including ears with an effusion) was present in 182 (7 5-2%) infected ears, reduced middle ear pressure (including ears with an effusion) in 217 (89.7%), and effusions in 155 (64%). Of the 155 effusions all but 17 were followed up until they had resolved (9 children did not attend for follow-up, 5 moved away from the area, and 3 became reinfected). Resolution of effusions was related to return of compliance reduction to normal, but abnormal pressure reduction was more long-lasting (table n). 50% and 90% of effusions had TABLE I-TYPES OF TYMPANOGRAM IN INFECTED AND

NON-INFECTED EARS AT PRESENTATION

TABLE II-RATES OF RESOLUTION OF EFFUSIONS, COMPLIANCE REDUCTION, AND PRESSURE REDUCTION IN INFECTED EARS

Types of tympanogram identified. Type I, effusion; type II, reduced pressure without effusion; type III, reduced compliance without effusion; type IV, compliance and pressure reduction without effusion; type V, Normal.

*The rate of resolution is calculated as the number of ears that had returned to normal at each time interval expressed as a percentage of the total-eg, 90% oi all effusions that resolved had resolved by the seventh week after presentation

531 TABLE III-COMPARISON OF THE RATES OF RESOLUTION OF

EFFUSION, COMPLIANCE REDUCTION, AND PRESSURE REDUCTION IN INFECTED AND NON-INFECTED EARS, IN EPISODES OF UNILATERAL OTITIS MEDIA

i

L-1i

I

i

I

TABLE IV-STATE OF THE MIDDLE EARS BEFORE INFECTION IN EPISODES OF REINFECTION

*This group comprises episodes in which tympanometry in the previous episodes was abnormal but patient had not been seen for three months.

by the end of the first and seventh week after presentation, respectively, and although one effusion lasted twenty-seven weeks and another thirty-one weeks, all ultimately resolved. In episodes of unilateral acute otitis media, 56 children (28’6%) had an effusion in the noninfected ear, 71 (36’2%) had compliance reduction (including ears with effusions) and 132 (67 - 3%) had pressure reduction (including ears with effusions). Effusions and compliance reduction returned to normal at resolved

about the same time in both infected and non-infected ears; pressure reduction returned to normal later but at the same time in both ears (table III). 41 children (26 - 607o) had more than 1 episode of acute otitis media. 26 children had 2 episodes and 8, 5 and 2 children had 3,4 and 5 episodes, respectively. 65episodes were reinfections in children who had had previous episodes of infection in the

study, and therefore the state of the ears was known before reinfection (table IV). A new effusion developed in 6 episodes just before reinfection and 3 episodes were a reinfection of an old effusion, which subsequently resolved satisfactorily (table IV). Those children with persistent or recurrent effusions were not at special risk of infection. Discussion In the few investigations of acute otitis media follow-up has been short. Qvarnberg,20 who tested infected ears 10 days after presentation and both infected and non-infected ears three months after presentation, found that effusions were present in 46 - 3% and 6 - 9% of ears, respectively; while Meistrup-Larsen et al. 21 tested infected and non-infected ears

weeks after presentation and found effusions in 41’ 3% of The resolution of effusions between the 1 Oth day and the third month identified by Qvarnberg is in accordance with the results of this study. Reves et al22 using tympanometry showed that children who had a presistent middle-ear effusion did not have a history of acute otitis media, suggesting that "glue ear" may not be a consequence of the disease. The present findings support this notion: 90% of effusions had resolved by the 7th week after presentation and none remained indefinitely. Anatomically and developmentally the middle-ear clefts may be regarded as extensions of the upper respiratory tract. The MRC survey of acute otitis media 23 concluded that the upper respiratory tract including the middle ears should be considered as a whole. The relation between the middle ears is demonstrated further here: in episodes of unilateral acute otitis media, middle ear changes were identified in both noninfected and infected ears, and the rate of resolution of each of the changes was almost the same irrespective of whether or not the ear had been infected. The fact that, after resolution of the acute infection, all the effusions ultimately resolved suggests that the middle-ear effusion that follows acute otitis media (even if present in the non-infected ear) is distinct from chronic serous otitis media or glue ear. This should be remembered when surgery is contemplated for a child with middle-ear effusion and a history of acute otitis media. This study has given no support to the theory that a persistent effusion predisposes to recurrent acute otitis media. Tympanometry has identified changes that have been described in the pathology of acute otitis media during the acute infection. However, because the incidence of types III and IV tympanograms was so small and because these types have also been associated with the presence of a middle-ear effusion, it was not possible to draw valid conclusions as to the inflammatory state or "stiffness" of the tympanic membrane and mucosa of the ossicular chain. That the rates of resolution of effusion and compliance reduction were similar is possibly due to the inaccuracy of compliance measurement, or an incorrect definition of compliance reduction. two

ears.

I thank Prof R. Harvard Davis, Department of General Practice, and Mr Richard Mills, Department of Surgery, University of Wales College of Medicine, for advice and criticism; Mr Geoff Hart, chief audiologist, University Hospital of Wales, for tuition in the use of the electro acoustic impedance bridge; Dr Edward Coles, Department of Medical Statistics, University of Wales College of Medicine, for advice on the storage and extraction of the study data; my partners, Dr Michael Richards, Dr Martin Harrison and Dr Helen Houston; and the study nurse, Mrs J. Skone. The study was funded by the Welsh Office, Welsh Scheme for the Development of Health and Social Research. Ampicillin was provided by Beecham Research Laboratories.

REFERENCES 1. Friedman I.

Pathology of the ear London: Blackwell Scientific Publications, 1974. 2. Mawson S Acute otitis media. Update 1971; (December): 1555-62 3. Sade J. Natural history of the secretory otitis media syndrome. In: Sade J, ed. Secretory otitis media and its sequalae. Edinburgh: Churchill Livingstone, 1979: 89-101. 4 Ballantyne J. Iatrogenic deafness. J Laryngol Otol 1970; October: 967-70. 5. Paparella MH. Pathogenesis of otitis media: panel discussion. Laryngoscope 1982, 92: 292-93. 6. Editorial. The glue-ear syndrome. Lancet 1975; i: 397. 7. Mawson S. Acoustic impedance measurements in diagnosis-discussion. Proc Roy Soc Med 1974; 67: 701-02 8. Black N Surgery for glue ear—a modern epidemic. Lancet 1984; i: 835-37. 9 Lowe JF, Bamforth JS, Pracy R. Acute otitis media-one year in general practice. Lancet 1963; ii: 1129-37. 10. Fry J, Dillane JB, McNab-Jones RF, Kalton G. The outcome of acute otitis media (A report to the Medical Research Council). Br J Prev Soc Med 1969; 23: 205-09. 11. Neil JF, Harrison SH, Morbey RD, Robinson GA, Tate GMT, Tate HT. Deafness in acute otitis media. Br Med 1966; i: 75-77. J

532 its effects. A chapter on "deteriorating stroke" is commendably practical but the newly coined term (p 123) must in practice be the least helpful, lumping recurrent embolism, progressing thrombosis, and rebleeding together with the complications of cerebral oedema, secondary effects on the heart and, above all, deterioration due to post-stroke depression. A special term that describes a circumstance calling for unusual or urgent intervention has a function. Other terms should not exist. These points bear witness to a certain idiosyncrasy. I think this is what the publishers mean by the "authors’ unique approach", and because of it the book is not for all physicians. It remains, nevertheless, an outstanding review by two acknowledged experts which, in my opinion, no physician who claims stroke as a special interest can afford to be without.

not

Reviews of Books The Acute Stroke Vladimir Hachinski, University of Western Ontario, London, Ontario, and John W. Norris, University of Toronto, Toronto, Ontario. Philadelphia: F. A. Davis. Beckenham: Quest-Meridien. 1985. Pp 286.

$56.25.

"No physician who treats stroke patients can afford to be without this book", is the claim on its cover. Acute stroke is shown not to be the single entity implied by use of the definite article, but otherwise the title says exactly what this book is about. That it is not about the treatment of stroke is quite clear: the long approach through 11 chapters of deeper matters-"the vascular infrastructure", reversibility of cerebral ischaemia, vascular syndromes, &cprepares for the dispatch of this aspect in just 13 pages. This order of things is not illogical but it brings problems. Diagnosis, for example, precedes investigation by 5 chapters. This is well excused by the authors’ emphasis on diagnosis as a clinical skill not dependent on investigations. More awkwardly, stroke presentations calling for special management-deteriorating stroke, young stroke-are covered long before basic principles of management. Considerable repetition is needed to overcome these difficulties. As a reference book, or perhaps a series of reviews, repetition serves it quite well: each chapter can stand on its own and the relations between chapters become less important. The depth of each is impressive, the presentations carefully discursive. Amongst a wealth of illustrations, some (the angiograms especially) would better serve their purpose if pertinent arrows assisted the legends. Both here and in the text, inexpert readers could be misled. There is strong dependence on data from the Toronto Stroke Unit which need to be seen in correct context as the authors are unhelpful in this respect. One example is the other syndromes mistaken for stroke (p 97), which in patients reaching a stroke unit are not the same as those seen at the doors of an accident and emergency department. Serological tests for syphilis may be "of doubtful value" (none positive in 1729 cases [p 191]) in a town that has been called "Toronto the Good", but you would not find that in London

(England). Clear guidelines to management of stroke never quite emerge. Again this is excused: considerations of benefit, cost, and risk "may indicate a different strategy for each individual" (p 222), but important uncertainties remain. The argument that a computerised tomographic scan should always be done is never conclusive, nor is the claim that "the principles of management depend upon knowing the precise underlying cause" (p 227), unfairly supported by citing the different management of subarachnoid haemorrhage, which is altogether a different illness. No consensus assists the use of terminology in progressing stroke, but the concept is surely one of progression of the underlying cause, Jeppsson PH, Nylen O, and Linden G. Audiological aspects of acute otitis media. Acta Otolaryngol 1973; 75: 439-42. 13. Brooks N. Acoustic impedance measurements in diagnosis Proc Roy Soc Med 1974; 67:

12.

698-701. 14. Alberti PW, Kristensen R. The clinical application of impedance audiometry. Laryngoscope 1970; 80: 735-46. 15. Linden G, Peterson JL, Björkman G. Tympanometry. Arch Otolaryngol 1970; 92: 248-57 16. Jerger J. Clinical experience with impedance audiometry. Arch Otolaryngol 1970, 92: 311-24. 17. Bluestone CD, Beery QC, Paradise JL. Audiometry and tympanometry in relation to middle ear effusions in children. Laryngoscope 1973; 83: 594-604. 18 Beery QC, Scott Andrus W, Bluestone CD, Cantekin EI Tympanometric pattern classification in relation to middle ear effusions. Ann Otol 1975; 84: 56-64. 19. Brooks DN. Hearing screening: a comparative study of an impedance method and pure tone screening. Scand Audio 1973; 2: 67-72 20. Qvarnberg Y. Acute otitis media. Acta Otolaryngol 1981; suppl 375. 21 Meistrup-Larsen KI, Sorensen H, Johnson NJ, Thomsen J, Myguid N, SederbergOlsen J. Two versus seven days penicillin treatment for acute otitis media. Acta Otolaryngol 1983; 96: 99-104 22. Reves R, Budgett R, Miller D, Wadsworth J, Haines A. Study of middle ear disease 290: 1953-56. using tympanometry in general practice. Br Med 1985; J 23. M.R.C. Survey Acute otitis media in general practice. Lancet 1957; ii: 510-14.

Academic Unit of Neurosaence, Charing Cross and Westminster Medical School, London

Health

T.J.STEINER

Consequences of Acute and Chronic Marihuana Use

Madelaine O.

Maykut, Health Protection Branch, Health and Welfare Canada, Ottawa, Ontario. Oxford: Pergamon. 1984. Pp. 328. 18. THE author states that she undertook this review because "a few attempts were made to write for the lay public which was an oversimplication so that scientists questioned statements made. A semi-lay-scientific effort was made when semantics caused some scientists to misinterpret the intended conclusions and implications. It was decided to do an original research literature search to find out why certain alleged controversies existed looking into the conditions of reported investigations such as subjects studied, materials used including potency, dose, route and/or mode of administration, frequency and duration of dose(s) used, previous drug(s) use, and state of health of subjects studied." Acknowledging that it would be impossible to cover the entire area of marihuana research in such a review, Miss Maykut has selected just under 400 references. Considerable technical information is included, but the presentation tends to report each study at length rather than employ a synthetic or critical approach which would assist the reader in understanding the controversies. By concentrating in some detail on reporting a rather limited number of reports, there must indeed be some selectivity, and the question is as to what criteria the author has employed to select. There is some internal evidence that the subject has been approached with the expectation that cannabis is a dangerous substance. While this is a perfectly reasonable view for someone to hold, it needs to be very carefully declared in a scientific review. In the body of the book, which contains references to many interesting papers, there are only three prior to 1970, two of which refer to teratogenetic effects of cannabis which have not been subsequently reported. The article by A. M. G. Campbell and colleagues in The Lancet in 1971 reporting the possibility of cerebral atrophy in young cannabis smokers is given considerable space, but without the subsequent discussion, also published, drawing attention to the unreliability of the ventricular studies then employed, and without noting Makyut’s earlier reservation that concomitant consumption of a range of other drugs could well explain any abnormal findings. Overall, the style of this book, while drawing attention to the adverse health consequences that might be related to acute and chronic marihuana use, cannot be recommended as a clear and synthetic scientific review, but could be of some value as a listing of scientific work alluding to such risks. Stonebow

Unit,

County Hospital,

MARTIN NUTCHESON

Hereford

New Editions

for Eye, Ear, Nose and Throat Surgery.-2nd ed. ByD Morrison, R. K. Mirakhur, and H. J. L, Craig. Edinburgh: Churchill Livingstone. 1985. Pp 210. 25. Clímcal Neurology for Psychiatnsts.-2nd ed. By D. M. Kaufman. Orlando Florida: Grune & Stratton. 1985. Pp 431.$44.50. Clinical Chemical Pathology.-lOth ed. By C. H. Gray, P. J. N. Howorth, any M. G. Rinsler. London: Edward Arnold. 1985. Pp 326. 8.00. Anaesthesia