ATELECTASIS AND SECRETORY OTITIS MEDIA
J. E.
SADE, M.D. BERCO,
M.D.
KFAR SABA, ISRAEL
SUMMARY - That condition where the tympanic membrane is displaced toward the promontory is termed atelectasis. Thirty-seven patients (61 ears) showing various degrees of atelectasis graded from stage 1 to stage 4 were studied. Atelectatic drums are an inflammatory phenomenon occurring in underventilated ears. This conclusion is reached by considering the reversibility of the atelectasis upon ventilation; while the inflammatory factor can be deduced from the history and histopathology of the atelectatic drum, as well as the histology of the necrosed incus, the latter occurs in over a third of Our cases. Also pneumatization of the mastoid is almost never present. Twelve (21%) of the ears treated did indeed develop a perforation at one time or another (two had cholesteatomas). Chronic granulating external otitis with specific features occurred in 15% of cases. The characteristics of these ears and their case histories lead us to view atelectatic ears as part of the otitis media syndrome, where their place is somehow transitional between secretory otitis media on the one hand and chronic otitis media on the other.
The pathological condition of displacement of the eardrum from its normal position toward the promontory is usually known as atelectatic ear. In the present study, an attempt is made to define and characterize this entity, which despite its common occurrence, is seldom discussed in detail or even referred to in current publications. METHODS AND MATERIALS
Thirty-seven patients who were found upon examination with the operating microscope to have one or both eardrums displaced medially towards the promontory are included in this study. The following information was recorded: 1. Degree and extent of drum displacement, i.e., degree of atelectasis. 2. Average age of patient. 3. Previous otologic history. 4. Frequency of nasal pathology and presence of adenoids. 5. Average extent of pneumatization. 6. Frequency and location of accompanying inflammation at time of examination. 7. Frequency of accompanying central perforation or cholesteatoma (or their development at later stage). 8. Frequency of association of middle ear effusion.
9. Frequency of ossicular lesions, particularly incus necrosis. 10. State of the other ear. 11. The incidence of atelectasis disappearance after insertion of a ventilating tube. 12. Period during which the. ventilating tube remained in position and what followed its extrusion. 13. Average hearing loss before and after insertion of ventilating tube. 14. Histopathology of the atelectatic tympanic membrane and the partially destroyed incuses. Seven tympanic membranes were removed at surgery and were examined histologically. The specimens were fixed in formalin, dehydrated in alcohol, and embedded in paraffin. Staining was performed with: 1) H. and E., 2) PAS, and 3) Weigert's elastin method. Three . incuses with various degrees of bony destruction were prepared for histological examination as above, after nitric acid decalcification. RESULTS
In the 37 patients (74 ears), 61 (82%) ears with tympanic membrane displacement to below the normal level were observed. In 21 patients (65%) the atelectasis occurred bilaterally. The collapsed tympanic membrane often seemed thin, at times transparent, or flabby. Degree of Tympanic Membrane Dis-
From the Meir Hospital, Kfar Saba, Israel, and the University of Iowa, Iowa City, Iowa.
66
67
ATELECTASIS
~CD STAGE
( Re t
ro ct e d ear)
u
0)
STAGE ( Atelectasis)
~CD STAGE
( Severe - retracti on)
W
Q
STAGE ( Adhesivl' otitis)
Fig. 1. Schematic representation of four stages of atelectatic ear.
placement (Fig. 1). In 17 ears (28%) the drum was found to be adherent to the promontory. This can be viewed as the extreme degree of displacement and is called "adhesive type" or stage 4. In 23 ears (37.5%) .the drum was found to be lying on the promontory, but not adhering to it; politzerization or touching the drum delicately with a suction tip showed that it could be raised. This can be viewed as a preceding state to stage 4 and is therefore termed stage 3 or "plastering." Twelve ears (19.5%) presented a collapsed drum touching the incus or stapes, but not the promontory. These can be considered as stage 2 or "severe retraction." Drums obviously retracted, but not yet touching the incus were seen in 9 ears (15%). This group was termed "retracted type" or stage 1. Extent of Retraction (Fig. 2). In 42 ears (69% ), the drum was totally displaced medially. These cases were termed "total atelectasis." Nineteen (31%)
of the patients showed various degrees of atelectasis of only part of the drum. These were termed "partial atelectasis." Of these, 17 showed atelectasis of the superior posterior quadrant, one of the central part of the drum and one of the anterior superior quadrant.
Other Observations. 1. The average age of the 37 patients was 30.7 years. 2. In 41 (67%) of the ears, otitis media (OM) was previously present, and secretory otitis media (SOM) in an equal number. 3. No obvious nasal pathology or allergy was observed in any of the patients. Adenoids were present in seven patients (11%), with an average age of 11 years, none of the adenoids was very large. 4. X-ray examination did not reveal that pneumatization had developed in any of the affected ears, the average air cell system was estimated as 1-2 cc (as compared with a maximal value of 30 and a mean of 15 cc). 5. In ten ears (16.5%) there was a chronic inflammatory state of the drum, often showing granulation. In nine (15%), small volcano-like granulations were present on the posterior canal wall (Fig. 2), near the annulus usually between the posterior superior and posterior inferior parts of the drum. (The frequent occurrence of granulations at this point, and its resemblance to a fort built by Herod the Great led us to refer to it in short as Herodion.) Quite often, a Herodion
HERODIO"
~
~
'%iiJ
T = Total
P=Partial
Fig. 2. Schematic representation of total and partial atelectasis of the drum as well as of the granulation tissue termed Herodion,
SAvt·BERCO
68
HERODION
r? ~\\\1I1111111111111111111111111111111111\1I11111111 ~:"
~ ~
s§If
~
IIIIIIII\~\~
DEAD
SPACE
Fig. 3. Schematic drawing of the dead space at the sinus tympani region created by an atelectatic pouch, with a Herodion just above it.
and a posterior superior atelectasis, stage 4 were found to be associated with a dead space created below the annulus at about the sinus tympani (Fig. 3). Such a dead space has little drainage or clearance facility, is therefore often infected and should be dealt with surgically. 6. Central perforations of the eardrum were present in eight cases when initially seen by us, while in an additional five patients a perforation developed with time. In four of the latter, a ventilating tube was introduced at one time or another before the perforation developed; however, the tube was usually introduced anterosuperiorly while the perforation developed centrally. Two cases presented themselves with an attic cholesteatoma, and another developed a shallow retraction pocket, (anterosuperior) which did not, however, develop further over the years into a true attic cholesteatoma. 7. Fifteen ears (24.5%) when initially seen were associated with a middle ear effusion. 8. Incus necrosis was present in over one-third of the ears (23 ears, 38%.) and was accompanied by stapes necrosis in five ears (8%). Some of the destroyed incuses were surrounded by granulation tissue, and the necrosis was not confined to the long process; the granulation tissue (and bony destruction) extended at times to the body of the incus and into the attic.
Fig. 4. Histologic section (H. and E.) of an atelectatic drum showing important inflammatory cell infiltration throughout all its layers.
9. Both ears were in an atelectatic state in 24 cases (63% ); chronic otitis media was present in the nonatelectatic ear in five cases (3.5% ) and tympanasclerosis in one case (2.5%). In only 19% of patients was the other ear normal. 10. Ventilating tubes were introduced into 28 ears with an intact chain; in 22, the drum returned to its normal position within one to three days. The ventilating tube remained in position for an average period of five months; however, the drum promptly collapsed to its previous position once the tube was extracted. The average hearing loss (with intact chain) was 27.3 dB before and 9 dB after introductionof the ventilating tube. 11. Fourteen patients were examined tympanometrically: Pressure measured was - 205 mm H 2 0 and an average impedance 3140. Histopatlwlof!,Y. The essential features observed 'in the tympanic membranes
ATELECTASIS
69
Fig. 5. Atelectatic drum showing progressive destruction and distortion of orientation of collagenous backbone, lesion being more pronounced towards center (right) of the drum. E - Epithelial side. Arrows - Collagenous middle layer. M - Mucosal side.
were inflammation of all the middle layers with significant destruction and disorientation of the normal pattern of the collagenous fibers (Figs. 4-8). Three incuses with various degrees of bony destruction showed inflammatory destruction as described previously.v" DISCUSSION
Terminology, Classification, Extent of Involvement and Grading. These are usually established as a means to identification, standardization of measurement and a basis for comparison with data of other workers. We regard the various degrees of tympanic membrane recession and displacement toward the promontory as belonging to the same clinicalpathological entity. The association of the terms retraction, severe retraction, plastering and adhesion with the four stages of displacement we have defined seem to us useful, especially when supplemented with descriptions of extent of involvement. Thus, when we report "partial atelectasis stage 3 with incus necrosis," the members of our team know precisely what was seen in a given ear. The Nature of the Atelectatic Ears. Our observations indicate that drum displacement is an inflammatory process which occurs in underventilated ears, suggesting much more than a casual relationship with the chronic otitis media (OM) group of conditions. The inflammatory component is demonstrated by the previous history in 66% of atelectatic ears of various forms of OM and SOM, the actual presence of some inflammatory
process and granulation tissue in some ( 15.5%), and associated chronic inflammatory processes in the other ear (16%). Indeed, the unmistakably inflammatory character of the histologic picture of the tympanic membrane and the damaged ossicles speaks for itself. Those ears in which no active inflammation was observed may have "burnt their inflammation out," whether the incus was found
Fig. 6. Enlargement of a section from Figure 5 showing that part of the collagenous middle layer which is relatively intact (arrow). Both layers, circular and radial, can be seen.
70
SAD£-BERCO
metic blockage of the Eustachian tube, resulting in a secondary negative pressure which "sucks" the drum inwards. However, the direct pressure measurements of Buckingham and Ferrer' showed rather low negative pressures (about 5 mm H 2 0 ), or the absence of negative pressure in over 25% of the cases of atelectatic ears they examined." Also, clearance from the tube in atelectatic ears shows free passage, 5 as also seen with politzerization. When atelectatic ears are operated upon, the middle ear and nasopharyngeal tubal openings are found to be normal. The adenoids are not enlarged, and are present only in young patients.
Fig. 7. Enlargement of a section from Figure 5 showing destruction and important disorientation of both collagenous layers (arrow).
to be eroded or not. Lack of mastoid pneumatization is indeed also characteristic of the chronic OM syndrome." The improvement in hearing and reexpansion of the drum in a large majority of these ears upon ventilation, and the collapse after extraction of the ventilating tube, is evidence of the underventilated state of these ears. The tympanic membrane, however, will not return to its proper position upon ventilation when it is adherent to the promontory (i.e., stage 4), and it is in these cases that ossicular erosion is most often present. Both ossicular pathology and tympanic membrane adhesion are secondary to more active or advanced inflammation, which is often accompanied by the presence of ~ranulations. The Pat1wgenesis of Atelectasis. Displacement of the tympanic membrane toward the promontory has been considered as essentially secondary to her-
Nevertheless, it is clear that underaeration of the middle ear, a major factor in atelectatic ears, is a secondary effect of tubal dysfunction or "insufficiency." This tubal dysfunction is probably a more complicated defect than "blockage" of the tube. At this time, we do not know the mechanism of this tubal dysfunction or how the amount of tympanic air deficit (underaeration) produces the retraction of the tympanic membrane. While underaeration of the middle ear is a necessary factor in atelectasis, it is not a sufficient factor to cause collapse of the tympanic membrane; underaeration is seen in other situations as well, such as SOM. The complementary factor would seem to be an alteration of the mechanical properties of the drum, such as destruction of the architecture of the collagenous backbone, secondary to inflammation, as was observed histologically.
The Atelectatic Ear and Otitis Media. Only a careful, prospective epidemiological study could reveal the sequential steps in inflammatory diseases of the middle ear. At the present stage, it would seem that the various forms of OM are in some degree related, sequentially, to one another, and have as a common denominator bacterial infection "seated" in an underventilated ear.
"This is in contrast to the negative pressures of hundreds of millimeters of water usually reported from tympanometric measurements. The discrepancy is due probably to the indirect nature of the tympanometric measurement technique. The direct measurements are clearly more meaningful.
ATELECTASIS
71
Fig. 8. Enlargement of a section from Figure 5 showing almost total disappearance of collagenous midlayers (arrow).
Acute OM is a disease of infancy and early childhood which attacks as many as 80% of children before the age of six," before they have immunological reactivity. Secretory otitis media, which is often a sequel to acute otitis media or upper respiratory infection, is mostly seen in young children. While Fabritzius" prospective study and Cohen's" thesis attest to the fact that patients with most SOM heal spontaneously, some do not recover as readily. These are probably the ears with more severe ventilating problems and some may show transformation in time to another form of the same disease, i.e., atelectatic ear. This may be deduced from the frequent preceding episodes of SOM as well as the findings in Fabritzius' study.' Simple chronic OM is an infection of the middle ear associated with perforation of its tympanic membrane. This occurs as a sequel to various previous assaults such as acute OM, trauma, and probably also atelectatic ear, and many patients do not really know or remember how the disease started. The 13 ears in our series which developed a perforation might well belong to the group of patients who developed chronic OM, but can remember no preceding infection." Neither the mechanism of perforation in
atelectatic ear nor the mechanism of the atrophy of the drum are known. (One might indeed term such a perforated drum as "atelectasis stage 5.") It is noteworthy that the frequency of incus necrosis observed by us, about one-third of the atelectatic ears, is very similar to that seen in chronic OM.1 Of special interest are the granulations seen over and near the atelectatic tympanic membrane and the regularity of the isolated Herodion. This phenomenon may be related to a clearance deficiency of keratin from the external auditory canal which might by itself be connected with the pathogenesis of chronic OM. Similar granulations, atelectasis, and recurrence of perforation were observed by us as a late phenomenon in otherwise successful tympanoplasty and myringoplasty; these cases revert, to some extent, to their original preoperative state through a basic uncorrected pathogenic defect. Treatment. Treatment of an atelectatic ear consists of aerating the middle ear and reconstructing the ossicular chain, or the tympanic membrane, or both, when necessary. Aeration of the middle ear to supplement the patient's inadequate auditory tube can be achieved by using a ventilating tube. An alternative is a perma-
72
SADE-BERCO
nent perforation, indeed, I have heard it remarked that a central perforation is God's own physiologic ventilating tube.!? It should be emphasized that a ventilating tube is not really satisfactory as the tube is almost always extruded and has to be reinserted frequently. The ideal solution would be to overcome Eustachian tube dysfunction. This, however, is not in sight. Ossicular chain interruption is encountered in two different situations:
1. The drum is intact, lying over the stapes; i.e., natural tympano-stapediopexy (or using old nomenclature, natural tympanoplasty, type III). We encountered this situation in eight out of the 23 cases with incus necrosis. In such cases, hearing might be satisfactory, inflammatory reaction has at times sub-
sided and nothing should be done. Indeed, this does not mean that once tubal insufficiency is present it will always be present. 2. In 23 cases (38%) of our series, there was incus necrosis with interruption of the ossicular chain, while 13 ears (21%) showed or developed tympanic membrane perforations. Most of these cases should be operated upon, repairing h dru db' h I t e man rmging t e one stapes in contact with the malleus, as in tympanoplasty surgery. However, the middIe ear requires ventilation and a tube is, therefore, inserted into the repaired drum. When the ventilating tube falls out, retraction may reappear, but this is not always the case; again reminding us that such tubal insufficiency might not be a permanent functional defect.
REFERENCES 6. Brownlee RC, De Loache VR, Cowan CC, et al: Otitis media in children. J Pediatr 75:636-642, 1969
1. Sade J, Berea E: Bone destruction in chronic otitis media. J Laryngol Otol 88:413422, 1974 2. Sade J, Halevy A: The aetiology of bone destruction in chronic otitis media. J Laryngol Otol 88:139-143, 1974
3. Diamant M: Chronic Otitis Basal. New York, S Karger, 1952 4. Buckingham RA, Ferrer JL: Middle ear pressures in Eustachian tube malfunction: Manometric studies. Laryngoscope 83: 15851593, 1973 5. Sade J, Hadas E: Eustachian tube clearance in health and disease. To be published.
7. Fabritzius HF: Hearing investigations of school children in North Trondelag County. J Oslo City Hosp 18:3-44, 1968 8. Cohen D: Secretory Otitis Media, thesis. Hebrew University, Jerusalem, 1968 9. Sade J, Halevy A: The natural history of chronic otitis media. J Laryngol Otol, to be published 10. Ingelstedt S. Personal communication, 1973
REPIUNTs - Jacob Sade, M.D., Meir Hospital, Kfar Saba, Israel. Dr. Sade is an Established Investigator of the Chief Scientist's Bureau, Ministry of Health, Meir Hospital and Weizmann Institute of Science, Israel. He is Visiting Professor in the Department of Otolaryngology and Maxillofacial Surgery, University of Iowa, Iowa City, Iowa, until July 1, 1976.
J. E.
SADE, M.D. BERCO,
M.D.
KFAR SABA, ISRAEL
SUMMARY - That condition where the tympanic membrane is displaced toward the promontory is termed atelectasis. Thirty-seven patients (61 ears) showing various degrees of atelectasis graded from stage 1 to stage 4 were studied. Atelectatic drums are an inflammatory phenomenon occurring in underventilated ears. This conclusion is reached by considering the reversibility of the atelectasis upon ventilation; while the inflammatory factor can be deduced from the history and histopathology of the atelectatic drum, as well as the histology of the necrosed incus, the latter occurs in over a third of Our cases. Also pneumatization of the mastoid is almost never present. Twelve (21%) of the ears treated did indeed develop a perforation at one time or another (two had cholesteatomas). Chronic granulating external otitis with specific features occurred in 15% of cases. The characteristics of these ears and their case histories lead us to view atelectatic ears as part of the otitis media syndrome, where their place is somehow transitional between secretory otitis media on the one hand and chronic otitis media on the other.
The pathological condition of displacement of the eardrum from its normal position toward the promontory is usually known as atelectatic ear. In the present study, an attempt is made to define and characterize this entity, which despite its common occurrence, is seldom discussed in detail or even referred to in current publications. METHODS AND MATERIALS
Thirty-seven patients who were found upon examination with the operating microscope to have one or both eardrums displaced medially towards the promontory are included in this study. The following information was recorded: 1. Degree and extent of drum displacement, i.e., degree of atelectasis. 2. Average age of patient. 3. Previous otologic history. 4. Frequency of nasal pathology and presence of adenoids. 5. Average extent of pneumatization. 6. Frequency and location of accompanying inflammation at time of examination. 7. Frequency of accompanying central perforation or cholesteatoma (or their development at later stage). 8. Frequency of association of middle ear effusion.
9. Frequency of ossicular lesions, particularly incus necrosis. 10. State of the other ear. 11. The incidence of atelectasis disappearance after insertion of a ventilating tube. 12. Period during which the. ventilating tube remained in position and what followed its extrusion. 13. Average hearing loss before and after insertion of ventilating tube. 14. Histopathology of the atelectatic tympanic membrane and the partially destroyed incuses. Seven tympanic membranes were removed at surgery and were examined histologically. The specimens were fixed in formalin, dehydrated in alcohol, and embedded in paraffin. Staining was performed with: 1) H. and E., 2) PAS, and 3) Weigert's elastin method. Three . incuses with various degrees of bony destruction were prepared for histological examination as above, after nitric acid decalcification. RESULTS
In the 37 patients (74 ears), 61 (82%) ears with tympanic membrane displacement to below the normal level were observed. In 21 patients (65%) the atelectasis occurred bilaterally. The collapsed tympanic membrane often seemed thin, at times transparent, or flabby. Degree of Tympanic Membrane Dis-
From the Meir Hospital, Kfar Saba, Israel, and the University of Iowa, Iowa City, Iowa.
66
67
ATELECTASIS
~CD STAGE
( Re t
ro ct e d ear)
u
0)
STAGE ( Atelectasis)
~CD STAGE
( Severe - retracti on)
W
Q
STAGE ( Adhesivl' otitis)
Fig. 1. Schematic representation of four stages of atelectatic ear.
placement (Fig. 1). In 17 ears (28%) the drum was found to be adherent to the promontory. This can be viewed as the extreme degree of displacement and is called "adhesive type" or stage 4. In 23 ears (37.5%) .the drum was found to be lying on the promontory, but not adhering to it; politzerization or touching the drum delicately with a suction tip showed that it could be raised. This can be viewed as a preceding state to stage 4 and is therefore termed stage 3 or "plastering." Twelve ears (19.5%) presented a collapsed drum touching the incus or stapes, but not the promontory. These can be considered as stage 2 or "severe retraction." Drums obviously retracted, but not yet touching the incus were seen in 9 ears (15%). This group was termed "retracted type" or stage 1. Extent of Retraction (Fig. 2). In 42 ears (69% ), the drum was totally displaced medially. These cases were termed "total atelectasis." Nineteen (31%)
of the patients showed various degrees of atelectasis of only part of the drum. These were termed "partial atelectasis." Of these, 17 showed atelectasis of the superior posterior quadrant, one of the central part of the drum and one of the anterior superior quadrant.
Other Observations. 1. The average age of the 37 patients was 30.7 years. 2. In 41 (67%) of the ears, otitis media (OM) was previously present, and secretory otitis media (SOM) in an equal number. 3. No obvious nasal pathology or allergy was observed in any of the patients. Adenoids were present in seven patients (11%), with an average age of 11 years, none of the adenoids was very large. 4. X-ray examination did not reveal that pneumatization had developed in any of the affected ears, the average air cell system was estimated as 1-2 cc (as compared with a maximal value of 30 and a mean of 15 cc). 5. In ten ears (16.5%) there was a chronic inflammatory state of the drum, often showing granulation. In nine (15%), small volcano-like granulations were present on the posterior canal wall (Fig. 2), near the annulus usually between the posterior superior and posterior inferior parts of the drum. (The frequent occurrence of granulations at this point, and its resemblance to a fort built by Herod the Great led us to refer to it in short as Herodion.) Quite often, a Herodion
HERODIO"
~
~
'%iiJ
T = Total
P=Partial
Fig. 2. Schematic representation of total and partial atelectasis of the drum as well as of the granulation tissue termed Herodion,
SAvt·BERCO
68
HERODION
r? ~\\\1I1111111111111111111111111111111111\1I11111111 ~:"
~ ~
s§If
~
IIIIIIII\~\~
DEAD
SPACE
Fig. 3. Schematic drawing of the dead space at the sinus tympani region created by an atelectatic pouch, with a Herodion just above it.
and a posterior superior atelectasis, stage 4 were found to be associated with a dead space created below the annulus at about the sinus tympani (Fig. 3). Such a dead space has little drainage or clearance facility, is therefore often infected and should be dealt with surgically. 6. Central perforations of the eardrum were present in eight cases when initially seen by us, while in an additional five patients a perforation developed with time. In four of the latter, a ventilating tube was introduced at one time or another before the perforation developed; however, the tube was usually introduced anterosuperiorly while the perforation developed centrally. Two cases presented themselves with an attic cholesteatoma, and another developed a shallow retraction pocket, (anterosuperior) which did not, however, develop further over the years into a true attic cholesteatoma. 7. Fifteen ears (24.5%) when initially seen were associated with a middle ear effusion. 8. Incus necrosis was present in over one-third of the ears (23 ears, 38%.) and was accompanied by stapes necrosis in five ears (8%). Some of the destroyed incuses were surrounded by granulation tissue, and the necrosis was not confined to the long process; the granulation tissue (and bony destruction) extended at times to the body of the incus and into the attic.
Fig. 4. Histologic section (H. and E.) of an atelectatic drum showing important inflammatory cell infiltration throughout all its layers.
9. Both ears were in an atelectatic state in 24 cases (63% ); chronic otitis media was present in the nonatelectatic ear in five cases (3.5% ) and tympanasclerosis in one case (2.5%). In only 19% of patients was the other ear normal. 10. Ventilating tubes were introduced into 28 ears with an intact chain; in 22, the drum returned to its normal position within one to three days. The ventilating tube remained in position for an average period of five months; however, the drum promptly collapsed to its previous position once the tube was extracted. The average hearing loss (with intact chain) was 27.3 dB before and 9 dB after introductionof the ventilating tube. 11. Fourteen patients were examined tympanometrically: Pressure measured was - 205 mm H 2 0 and an average impedance 3140. Histopatlwlof!,Y. The essential features observed 'in the tympanic membranes
ATELECTASIS
69
Fig. 5. Atelectatic drum showing progressive destruction and distortion of orientation of collagenous backbone, lesion being more pronounced towards center (right) of the drum. E - Epithelial side. Arrows - Collagenous middle layer. M - Mucosal side.
were inflammation of all the middle layers with significant destruction and disorientation of the normal pattern of the collagenous fibers (Figs. 4-8). Three incuses with various degrees of bony destruction showed inflammatory destruction as described previously.v" DISCUSSION
Terminology, Classification, Extent of Involvement and Grading. These are usually established as a means to identification, standardization of measurement and a basis for comparison with data of other workers. We regard the various degrees of tympanic membrane recession and displacement toward the promontory as belonging to the same clinicalpathological entity. The association of the terms retraction, severe retraction, plastering and adhesion with the four stages of displacement we have defined seem to us useful, especially when supplemented with descriptions of extent of involvement. Thus, when we report "partial atelectasis stage 3 with incus necrosis," the members of our team know precisely what was seen in a given ear. The Nature of the Atelectatic Ears. Our observations indicate that drum displacement is an inflammatory process which occurs in underventilated ears, suggesting much more than a casual relationship with the chronic otitis media (OM) group of conditions. The inflammatory component is demonstrated by the previous history in 66% of atelectatic ears of various forms of OM and SOM, the actual presence of some inflammatory
process and granulation tissue in some ( 15.5%), and associated chronic inflammatory processes in the other ear (16%). Indeed, the unmistakably inflammatory character of the histologic picture of the tympanic membrane and the damaged ossicles speaks for itself. Those ears in which no active inflammation was observed may have "burnt their inflammation out," whether the incus was found
Fig. 6. Enlargement of a section from Figure 5 showing that part of the collagenous middle layer which is relatively intact (arrow). Both layers, circular and radial, can be seen.
70
SAD£-BERCO
metic blockage of the Eustachian tube, resulting in a secondary negative pressure which "sucks" the drum inwards. However, the direct pressure measurements of Buckingham and Ferrer' showed rather low negative pressures (about 5 mm H 2 0 ), or the absence of negative pressure in over 25% of the cases of atelectatic ears they examined." Also, clearance from the tube in atelectatic ears shows free passage, 5 as also seen with politzerization. When atelectatic ears are operated upon, the middle ear and nasopharyngeal tubal openings are found to be normal. The adenoids are not enlarged, and are present only in young patients.
Fig. 7. Enlargement of a section from Figure 5 showing destruction and important disorientation of both collagenous layers (arrow).
to be eroded or not. Lack of mastoid pneumatization is indeed also characteristic of the chronic OM syndrome." The improvement in hearing and reexpansion of the drum in a large majority of these ears upon ventilation, and the collapse after extraction of the ventilating tube, is evidence of the underventilated state of these ears. The tympanic membrane, however, will not return to its proper position upon ventilation when it is adherent to the promontory (i.e., stage 4), and it is in these cases that ossicular erosion is most often present. Both ossicular pathology and tympanic membrane adhesion are secondary to more active or advanced inflammation, which is often accompanied by the presence of ~ranulations. The Pat1wgenesis of Atelectasis. Displacement of the tympanic membrane toward the promontory has been considered as essentially secondary to her-
Nevertheless, it is clear that underaeration of the middle ear, a major factor in atelectatic ears, is a secondary effect of tubal dysfunction or "insufficiency." This tubal dysfunction is probably a more complicated defect than "blockage" of the tube. At this time, we do not know the mechanism of this tubal dysfunction or how the amount of tympanic air deficit (underaeration) produces the retraction of the tympanic membrane. While underaeration of the middle ear is a necessary factor in atelectasis, it is not a sufficient factor to cause collapse of the tympanic membrane; underaeration is seen in other situations as well, such as SOM. The complementary factor would seem to be an alteration of the mechanical properties of the drum, such as destruction of the architecture of the collagenous backbone, secondary to inflammation, as was observed histologically.
The Atelectatic Ear and Otitis Media. Only a careful, prospective epidemiological study could reveal the sequential steps in inflammatory diseases of the middle ear. At the present stage, it would seem that the various forms of OM are in some degree related, sequentially, to one another, and have as a common denominator bacterial infection "seated" in an underventilated ear.
"This is in contrast to the negative pressures of hundreds of millimeters of water usually reported from tympanometric measurements. The discrepancy is due probably to the indirect nature of the tympanometric measurement technique. The direct measurements are clearly more meaningful.
ATELECTASIS
71
Fig. 8. Enlargement of a section from Figure 5 showing almost total disappearance of collagenous midlayers (arrow).
Acute OM is a disease of infancy and early childhood which attacks as many as 80% of children before the age of six," before they have immunological reactivity. Secretory otitis media, which is often a sequel to acute otitis media or upper respiratory infection, is mostly seen in young children. While Fabritzius" prospective study and Cohen's" thesis attest to the fact that patients with most SOM heal spontaneously, some do not recover as readily. These are probably the ears with more severe ventilating problems and some may show transformation in time to another form of the same disease, i.e., atelectatic ear. This may be deduced from the frequent preceding episodes of SOM as well as the findings in Fabritzius' study.' Simple chronic OM is an infection of the middle ear associated with perforation of its tympanic membrane. This occurs as a sequel to various previous assaults such as acute OM, trauma, and probably also atelectatic ear, and many patients do not really know or remember how the disease started. The 13 ears in our series which developed a perforation might well belong to the group of patients who developed chronic OM, but can remember no preceding infection." Neither the mechanism of perforation in
atelectatic ear nor the mechanism of the atrophy of the drum are known. (One might indeed term such a perforated drum as "atelectasis stage 5.") It is noteworthy that the frequency of incus necrosis observed by us, about one-third of the atelectatic ears, is very similar to that seen in chronic OM.1 Of special interest are the granulations seen over and near the atelectatic tympanic membrane and the regularity of the isolated Herodion. This phenomenon may be related to a clearance deficiency of keratin from the external auditory canal which might by itself be connected with the pathogenesis of chronic OM. Similar granulations, atelectasis, and recurrence of perforation were observed by us as a late phenomenon in otherwise successful tympanoplasty and myringoplasty; these cases revert, to some extent, to their original preoperative state through a basic uncorrected pathogenic defect. Treatment. Treatment of an atelectatic ear consists of aerating the middle ear and reconstructing the ossicular chain, or the tympanic membrane, or both, when necessary. Aeration of the middle ear to supplement the patient's inadequate auditory tube can be achieved by using a ventilating tube. An alternative is a perma-
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nent perforation, indeed, I have heard it remarked that a central perforation is God's own physiologic ventilating tube.!? It should be emphasized that a ventilating tube is not really satisfactory as the tube is almost always extruded and has to be reinserted frequently. The ideal solution would be to overcome Eustachian tube dysfunction. This, however, is not in sight. Ossicular chain interruption is encountered in two different situations:
1. The drum is intact, lying over the stapes; i.e., natural tympano-stapediopexy (or using old nomenclature, natural tympanoplasty, type III). We encountered this situation in eight out of the 23 cases with incus necrosis. In such cases, hearing might be satisfactory, inflammatory reaction has at times sub-
sided and nothing should be done. Indeed, this does not mean that once tubal insufficiency is present it will always be present. 2. In 23 cases (38%) of our series, there was incus necrosis with interruption of the ossicular chain, while 13 ears (21%) showed or developed tympanic membrane perforations. Most of these cases should be operated upon, repairing h dru db' h I t e man rmging t e one stapes in contact with the malleus, as in tympanoplasty surgery. However, the middIe ear requires ventilation and a tube is, therefore, inserted into the repaired drum. When the ventilating tube falls out, retraction may reappear, but this is not always the case; again reminding us that such tubal insufficiency might not be a permanent functional defect.
REFERENCES 6. Brownlee RC, De Loache VR, Cowan CC, et al: Otitis media in children. J Pediatr 75:636-642, 1969
1. Sade J, Berea E: Bone destruction in chronic otitis media. J Laryngol Otol 88:413422, 1974 2. Sade J, Halevy A: The aetiology of bone destruction in chronic otitis media. J Laryngol Otol 88:139-143, 1974
3. Diamant M: Chronic Otitis Basal. New York, S Karger, 1952 4. Buckingham RA, Ferrer JL: Middle ear pressures in Eustachian tube malfunction: Manometric studies. Laryngoscope 83: 15851593, 1973 5. Sade J, Hadas E: Eustachian tube clearance in health and disease. To be published.
7. Fabritzius HF: Hearing investigations of school children in North Trondelag County. J Oslo City Hosp 18:3-44, 1968 8. Cohen D: Secretory Otitis Media, thesis. Hebrew University, Jerusalem, 1968 9. Sade J, Halevy A: The natural history of chronic otitis media. J Laryngol Otol, to be published 10. Ingelstedt S. Personal communication, 1973
REPIUNTs - Jacob Sade, M.D., Meir Hospital, Kfar Saba, Israel. Dr. Sade is an Established Investigator of the Chief Scientist's Bureau, Ministry of Health, Meir Hospital and Weizmann Institute of Science, Israel. He is Visiting Professor in the Department of Otolaryngology and Maxillofacial Surgery, University of Iowa, Iowa City, Iowa, until July 1, 1976.
