Middle Ear Cleft Opacification in Acute Otitis Externa: Sequela or Incidentaloma?

Introduction

In the differential diagnosis of otalgia, ear fullness, and hearing impairment, acute otitis externa (AOE) and acute otitis media represent distinct clinical entities with different pathophysiology and treatment protocols. Diagnosis becomes more challenging when imaging performed on patients diagnosed with unresolved or complicated AOE reveals middle ear cleft opacification (MECO), blurring the lines between these conditions—does the patient indeed suffer from AOE, a complication of AOE, or middle ear (ME) pathology? This overlap raises the question of whether AOE routinely leads to ME and mastoid effusion, and if these occurrences require any clinical attention.

AOE, by textbook definition, is restricted to the realm of the external auditory canal (EAC). ¹ Anatomically, the external ear is separated from ME by the tympanic membrane (TM), a 3-layered structure consisting of an external epithelial layer, a central fibrous layer, and an internal mucosal layer. The TM has been traditionally seen as an anatomic barrier, suggesting that inflammatory processes within the EAC wouldn’t typically involve the ME. Yet, otolaryngology consultations often involve cases of ME effusion following AOE. A general practitioner encountering a post-AOE patient with ME effusion, especially if describes aural fullness or hearing impairment, might consider antibiotic treatment continuation and referral for an otolaryngology consultation to rule out ME involvement or AOE deterioration. Radiologists who encounter ME opacification in AOE patients will typically recommend an otolaryngology consultation for clinical correlation.

Current literature is scant on the interplay between inflammation of the EAC and subsequent impacts on the ME cleft. Conversely, considerable research has focused on the high rate of radiological incidental findings of ME and mastoid opacifications in asymptomatic individuals.^{2 -9} Whether a MECO in post-AOE patients is related to the AOE or incidental, is unclear. Therefore, this study’s aim is to determine the rate and characteristics of MECO post-AOE.

Methods

The present study received clearance from our Institutional Review Board, 0161-22-RMB. Informed consent was waived due to the retrospective nature of the study. Our cohort included patients diagnosed with AOE at our otolaryngology acute care facility within a tertiary center. AOE was diagnosed clinically by symptoms of otalgia, ear fullness, or hearing impairment, with physical examination revealing redness and swelling of the EAC accompanied by discharge. The EAC was cleaned of discharge to facilitate adequate visualization of the TM and to rule out the presence of ME pathology or TM perforation.

In addition to their admission for AOE, all study participants were readmitted to our hospital acute care facility within the study period. During this subsequent admission, they underwent brain imaging within 3 months following the onset of AOE symptoms, for reasons unrelated to AOE management. This selection criterion allowed us to evaluate the ME condition in standard cases of AOE, enabling a broader understanding of the phenomenon beyond just the severe instances. Furthermore, this approach ensured the exclusion of necrotizing otitis externa cases, in which imaging is typically performed due to the severity of symptoms and physical findings, and ME and mastoid opacification are expected features. The 3-month duration limit was selected based on the typical resolution time of ME effusion within this period and to minimize confounding factors that could affect the radiologic findings of MECO.

Exclusion criteria included patients under 13 years of age, due to the high prevalence of otitis media with effusion (OME) in school-aged children,^10,11 patients exhibiting symptoms of otalgia or persistent ear discharge at the time of imaging, and documentation of concurrent or previous medical records regarding prior acute or chronic otitis media, cholesteatoma, chronic AOE, bilateral AOE, TM perforation, EAC wall dehiscence, temporal bone erosions, soft tissue extension, temporal bone abscess, temporal bone trauma, head and neck malignancies, and EAC anatomic malformations.

Imaging studies were independently evaluated by a neuroradiology specialist, who was blinded to the patients’ clinical data. A control group, consisting of the healthy contralateral (CL) ears from the same participants, was established for interpatient comparisons. The incidence of MECO (MECO as a proportion of all AOE cases) was assessed. Furthermore, the grade of MECO was systematically categorized as no opacification, partial opacification, or total opacification (Figure 1).

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Figures 1.

Axial and coronal CT scans demonstrating MECO grades. (A-C) Coronal CT scans illustrating the ME condition: (A) Clear ME, (B) Partially opacified ME, and (C) completely opacified ME. (D-F) Axial CT scans depicting the mastoid states: (D) Clear mastoid, (E) Partially opacified mastoid, and (F) completely opacified mastoid.

The outcomes were analyzed in relation to 2 dimensions:

Additionally, we performed a comparative analysis of the demographic, clinical, and radiologic features between patients with MECO and those without. Parameters included were patient age, diabetes rate, oral and intravenous treatment prescribed during AOE diagnosis, imaging indication (trauma vs neurologic), and mastoid pneumatization grade. The latter was included considering various mechanisms of ME aeration that might influence opacification rates and was graded based on the classification by Han et al ¹² : hypo-pneumatization, moderate, good, and hyper-pneumatization.

Data was analyzed with SPSS Statistics 27.0 software. The P-value of <.05 was considered statistically significant for all analyses. Descriptive statistics were performed using median, standard deviation, and range. Categorical variables were presented as frequencies. The chi-square test examined the difference in the MECO rates between the affected and contralateral (CL) ears within individuals. Further analysis was used to explore the relationship between the outcome of MECO and patients’ characteristics.

Results

Temporal Dimension of MECO Post-AOE

Up to 3 months after AOE symptoms onset, the opacification rate in the AOE ears was 38.0% (35/92) and 10.8% (10/92) in the CL ear (χ²[1, N = 92] = 8.379, P = .004). The rate of MECO in AOE ears was 58.9% (23/39) following 2 weeks, 28.5% (8/28) following 1 month, and 8.0% (2/25) following 3 months (Figure 2). MECO rates in CL ear were 12.8% (5/39) following 2 weeks, 17.2% (5/29) following 1 month, and 8.0% (2/25) following 3 months. The overall incidence of complete opacification decreased over time; Rates of complete opacification in AOE ears were 25.6% (10/39), 10.7% (3/28), and 0% (0/25), following 2 weeks, 1 month, and 3 months, respectively (Figure 3). The rate of partial opacification increased accordingly.

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Figure 2.

Dynamics of middle ear cleft opacification following AOE. The rate of MECO in AOE ears was 58.9% (23/39) following 2 weeks, 28.5% (8/28) following 1 month, and 8.0% (2/25) following 3 months (Figure 2). MECO rates in CL ear were 12.8% (5/39) following 2 weeks, 17.2% (5/29) following 1 month, and 8.0% (2/25) following 3 months.

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Figure 3.

Rates and grades of MeMO subsequent to the onset of AOE symptoms, observed at 2 weeks, 1 month, and 3 months post-AOE symptoms onset. The x-axis tracks the time elapsed since symptom onset, and the y-axis represents the percentage of AOE cases exhibiting MECO. The MECO rates in AOE-affected ears were 58.9% (23/39) at 2 weeks, decreasing to 28.5% (8/28) at 1 month, and further to 8.0% (2/25) at 3 months. Bars colors distinguish between the grades of opacification; dark gray indicates total opacification, while light gray represents partial opacification. Complete opacification in AOE ears was noted in 25.6% (10/39) of cases at 2 weeks, declining to 10.7% (3/28) at 1 month, and 0% (0/18) at 3 months.

Anatomic Dimension of MECO Post-AOE

Sixty-five percent (23/35) of MECO exhibited opacification in both the ME and mastoid, 28.5% (10/35) showed isolated mastoid opacification, and 5.7% (2/35) demonstrated isolated ME opacification. Among all cases of ME opacification, sole epitympanic opacification occurred in 16.0% (4/25), followed by mesotympanic and hypotympanic opacification in 8.0% (2/25) and 4.0% (1/25), respectively (Table 1). In 64.0% (16/25) of the cases, opacification affected all parts of the ME.

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Table 1.

Anatomic Distribution of ME Cleft Opacification Following Acute Otitis Externa.

Mastoid (n, %)	Epitympanic (n, %)	Mesotympanic (n, %)	Hypotympanic (n, %)	All ME parts (n, %)
23, 65.7	4, 11.4	2, 5.7	1, 2.8	16, 45.7

Abbreviation: ME, middle ear.

Opacification predominantly seen in upper ME cleft (mastoid and epitympanum).

Discussion

Our data found elevated rates of MECO in adults and children above 13 years old, diagnosed with AOE, compared to the healthy CL ear. This suggests that AOE might surpass the EAC and initiate a reactive response in the ME and mastoid. A high incidence of total opacification was observed shortly after the resolution of AOE, which later transitioned to partial opacification. This trend in the rate and grade of opacification demonstrated a progressive decrease from the onset of symptoms up to 3 months, indicative of spontaneous resolution.

The pathophysiology of MECO following AOE is not obvious. Few studies have examined MECO in necrotizing otitis externa.^{13 -17} In such conditions, a compromised EAC and deviations from its typical anatomical confines could provide a plausible rationale for effusion reaching the ME and mastoid regions. However, the reasons behind MECO remain unclear in situations with intact anatomy, as in uncomplicated AOE. The literature lacks clinical studies about the effect of external ear inflammation on the ME. We found only 1 study that investigated ME opacification following AOE, involving 29 ears, in which the imaging was prompted by external otitis diagnosis, suggesting these were more severe or chronic instances necessitating radiologic evaluation. ¹⁸

The TM has been traditionally viewed as a defensive barrier against pathogens. A potential hypothesis to our findings is that it might actively facilitate the transmission of the inflammatory process. Animal research has identified 2 primary pathways to ME effusion following EAC irritation: vasoactive response and histamine release, leading to effusion from mast cells in the pars flaccida, causing predominantly epitympanic effusion.^19,20 In our study, effusion was mostly found in all ME parts, probably due to patients’ lying posture during the imaging scan. The notable incidence of mastoid opacification in our results, combined with the marginally higher epitympanic opacification, settled with the epitympanic involvement, given the anatomical linkage between the epitympanum and mastoid cavity through the aditus ad antrum. The complex anatomical connections between the mastoid air cells and the Eustachian tube may hinder efficient fluid clearance, thereby facilitating the prolonged presence of mastoid effusion and increasing its incidence.

Our study has clinical implications. It is well-established that ME effusion is a complication of acute otitis media, typically resolving spontaneously within 3 months and therefore typically involves follow-up only, without the need for medical treatment. Our results further suggest that OME is also a possible sequela of AOE. This sheds light on the natural history of these 2 common otolaryngological entities—AOE and OME. The course of this ME effusion is likely to disappear gradually and therefore, it is not indicative of AOE deterioration or ME inflammation. Consequently, in cases where physical examinations reveal no signs of acute inflammation, the potential risks and costs associated with the side effects of antibiotics can be avoided. This information is valuable for otolaryngologists as well as general practitioners who treat AOE and for radiologists who interpret such findings.

Our study has several limitations. Firstly, only 77.1% of the 92 patients arrived for a follow-up, which ensured AOE resolution. Secondly, an otoscopic examination was performed only in 54.2% of patients with MECO during imaging time. To address the potential influence of confounding factors on the occurrence of MECO, strict inclusion and exclusion criteria were applied to minimize the likelihood of another medical condition developing during the study period. Nevertheless, the possibility remains that a micro-perforation present during the acute phase of AOE was overlooked due to EAC swelling, purulence, and pain. To address this limitation, it is noteworthy that re-evaluation of patients during the second admission and at follow-up revealed a normal TM in all cases.

Additionally, our sample tended toward an older population, with 18.4% of patients diagnosed with diabetes. This skew results from our exclusion of pediatric patients below 13 years old due to the high rate of OME, from older or diabetic individuals’ increased likelihood of undergoing brain imaging due to neurologic condition, and from a general reluctance to expose younger individuals to CT imaging. Moreover, by concentrating on individuals who presented to the emergency room, our findings might disproportionately represent those with more severe cases of the condition.

Conclusions

ME effusion is a sequela of AOE that resolves spontaneously over time. Physical examinations or imaging revealing fluids in the ME cleft following AOE, without further signs of ME inflammation, are benign and don’t require any treatment. Further studies are needed to investigate the role of the pars flaccida in OME.