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20 Retraction Pockets andAdhesive Otitis Media
Fig. 20.8 Adhesive otitis
media in the left ear. M
mallues, I Incus, S Stapes,
P Promontorium
419
Signicant conductive hearing loss and recurrent infections mandate surgery.
Surgical options include elevation of the TM from the medial wall of the middle
ear, support with a cartilage graft, and insertion of a ventilation tube by puncturing the cartilage graft. The aim is to improve hearing and to obtain self-cleaning
ear canal skin. Success rates of up to 80% have been reported with this
method [32].
There is no need for treatment in stable patients without signicant hearing loss.
Hearing aids may be a good option for patients with only hearing loss no recurrent
discharge and no suspected cholesteatoma. However, with the use of hearing aids,
ventilation in the external auditory canal may deteriorate and humidity may increase.
Thus, the frequency of recurrent infections may increase.
The main goals of surgical treatment are to carefully remove all adherent epithelium from the posterior and medial wall, strengthen the atrophic membrane with
perichondrium and cartilage, provide a self-cleaning surface for the TM epithelium,
and properly ventilate the middle ear. The most difcult steps in these procedures
are the removal of the epithelium from the ossicular chain, over the round window,
and the sinuses in the posterior tympanic cavity. During these interventions, the risk
of sensorineural hearing loss and leaving squamous epithelium in the MEC is quite
high. In studies, the benet of surgery on hearing level reaches 83.6% [32, 33]. In
these studies, it has been reported that in order to obtain good results in the long
term, the MEC should continue to be ventilated with the application of a ventilation
tube or intervention to the ET.
In patients with AdOM complicated with cholesteatoma, the best surgical option
is canal wall-down mastoidectomy without removal of the adhesive tympanic membrane. In this option, the aim is to have an epithelial surface that will prevent the
accumulation of keratin debris.
420
B. Polat et al.
20.8 Conclusion
The major underlying problem in RP and AdOM is aeration disorder of the
MEC.The disease process is long, and serious destructive problems occur in the
later periods. The treatment of AdOM is particularly challenging. Therefore, preventive treatment is much more important.
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421
Complications ofOtitis Media
21
SerkanŞerifler, SuelaSallavaci,
andMahmutTayyarKalcioglu
21.1 Introduction
The use of antibiotics has led to a general reduction in the incidence of complications associated with otitis media compared with the time before antibiotics were
available [1]. However, serious complications can still occur. Some of these can be
associated with high mortality rates. Both acute and chronic otitis media can cause
intracranial and extracranial complications. Complications of otitis media are a
common challenge in developing countries [2]. These complications can be attributed to various factors such as socioeconomic inequalities, limited access to education, inadequate healthcare facilities, and lack of awareness of otological symptoms.
Conversely, in developed countries, the incidence of complications may be inuenced by factors such as antibiotic resistance, which hinders effective treatment,
and the use of antibiotics which can temporarily mask symptoms and lead to delayed
diagnosis. In addition, changes in the virulence of the causative microorganisms
may also play a role in the complications seen in developed countries [3].
Both acute otitis media (AOM) and chronic otitis media (COM) complications
have a similar classication named intracranial and extracranial complications.
Intratemporal and extratemporal complications are subdivisions of extracranial [2]
(Table 21.1). Among intratemporal complications, acute mastoiditis is the most
S. Şerier (*)
A life Hospital, Ankara, Turkey
S. Sallavaci
Department of Otorhinolaryngology, University Hospital Center “Mother Teresa”,
Tirana, Albania
M. T. Kalcioglu
Faculty of Medicine, Department of Otorhinolaryngology, Istanbul Medeniyet University,
Istanbul, Turkey
Goztepe Prof. Dr. Suleyman Yalcin City Hospital, ENT Clinic, Istanbul, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_21
423
424
S. Şerier et al.
Table 21.1 Complications
of otitis media
Extracranial Intratemporal:
Acute mastoiditis
Facial paralysis
Labyrinthitis
Labyrinth stula
Petrositis
Extratemporal:
Subperiosteal abscess
Bezold abscess
Luc abscess
Intracranial Meningitis
Lateral sinus thrombosis
Epidural abscess
Subdural empyema
Otitic hydrocephalus
Brain abscess
common. On the other hand, meningitis is recognized as the most common intracranial complication, while brain abscess has the highest mortality rate among complications [4]. It is worth noting that two or more complications may coexist.
The development of complications in otitis media depends on ve key elements:
the virulence of the infecting organism and its susceptibility to antibiotics, host
resistance, the effectiveness of antibiotic treatment, anatomical pathways and barriers that facilitate spread, and airspace drainage pathways [5]. In AOM, the primary
causative microorganisms are Streptococcus pneumoniae, Haemophilus inuenzae,
and Moraxella catarrhalis, whereas in COM, the pathogens observed include
Pseudomonas aeruginosa, Streptococcus aureus, Proteus, and Bacteroides. For
AOM, an appropriate choice of antibiotic is generally sufcient for treatment.
However, in COM, medical treatment alone may not be sufcient and surgery may
be required to clean the middle ear and mastoid region, remove the infection, and
ensure proper ventilation [6, 7]. In both AOM and COM, there are cases where
complications make surgery necessary. These situations will be discussed in the following sections.
Vigilance for early clinical signs is essential to prevent complications. Early
diagnosis and prompt treatment can prevent the onset or progression of many complications [8]. While other complications typically manifest in a subacute or chronic
manner, meningitis can occur abruptly without early clinical signs. Therefore, complications should be suspected if an otological infection persists for more than two
weeks [9]. The main clinical signs of complications in AOM are lethargy, altered
cognition, irritability (especially in the pediatric population) and fever that does not
improve despite antibiotic treatment. These symptoms require immediate attention
and further assessment for possible complications. In cases of COM with symptoms
such as foul-smelling discharge, pain, and high fever, the possibility of complications should be considered. Specic ndings may be indicative of certain complications. For example, retroorbital pain may suggest petrositis, whereas photophobia
21 Complications ofOtitis Media
425
and altered consciousness may suggest meningitis. Facial asymmetry may suggest
facial paralysis. Severe focal neurological signs may suggest a brain abscess, and
papilledema may indicate the presence of a brain abscess. Vertigo may be related to
labyrinthine problems [10].
The preferred imaging modality is contrast-enhanced computed tomography
(CT) to assess complications. Magnetic resonance imaging (MRI) is particularly
useful for intracranial complications [11]. Additional laboratory tests such as a
complete blood count, lumbar puncture, tympanocentesis and culture may also be
helpful in diagnosing complications. Lumbar puncture can help diagnose intracranial spread, but it’s important to rule out increased intracranial pressure and the risk
of herniation with imaging before the procedure [12].
21.2 Intratemporal Complications
21.2.1 Acute Mastoiditis
The most common complication of otitis media in the pediatric population is still
acute mastoiditis. Acute mastoiditis usually develops after AOM in the pediatric
population [13]. Bacteria from the middle ear may migrate into the air cells of the
mastoid bone. Less commonly, a cholesteatoma can block ear drainage and lead to
mastoiditis. The peak incidence is between 1 and 4years of age. Younger children
are susceptible to infection due to immunological deciencies that predispose them
to risk factors for otitis media, with an increased risk of progression to acute mastoiditis (Fig.21.1) [14, 15].
Post-auricular swelling, tenderness, erythema, and auricular protrusion are the
most common diagnostic signs. Mucosal inammation, granulation tissue, or cholesteatoma may cause occlusion of the aditus and posterior epitympanum, resulting
in impaired mastoid drainage and persistent disease in the mastoid. If untreated or
inadequately treated, the inammation crosses the mucosa and spreads through the
venous channels, causing inammation in the periosteum. As a result of this spread,
Fig. 21.1 Computed tomograhy images of acute mastoiditis
426
S. Şerier et al.
symptoms such as postauricular pain, erythema, and swelling develop. Acute mastoiditis with acute periostitis usually responds to appropriate antibiotic therapy.
Coalescent mastoiditis is characterized by the destruction of bony septa in the mastoid air cell trabeculae. In acute coalescent mastoiditis, pressurized purulent material in the mastoid air cells causes necrosis of the bone septa [13].
If the pain persists for up to 2weeks, the purulent discharge does not resolve, or
the complaints and ndings worsen, coalescent mastoiditis after AOM is suspected.
The most common presenting complaint is postauricular tenderness, which is present in most patients. If there is a perforation on otoscopy, purulent discharge may be
seen in the external ear canal. If there is no perforation, effusion may be seen in the
middle ear behind the tympanic membrane. However, the tympanic membrane and
middle ear may appear normal in the presence of aditus obstruction. Induration and
erythema on the mastoid bone may be a sign of a subperiosteal abscess. If the infection erodes through the lateral cortex of the mastoid medial to the insertion of the
sternocleidomastoid muscle, it is known as Bezold’s abscess. Acute mastoiditis is
usually caused by S. pneumoniae, S. pyogenes, S. aureus, and H. inuenzae [16]. CT
is the main diagnostic tool. Once acute mastoiditis has been diagnosed, aggressive
treatment is required. All patients are started on antibiotics on admission. In patients
who do not respond, the rst step is to perform a myringotomy, take a culture and,
if necessary, insert a ventilation tube. Antibiotics are then given according to the
results of the culture. If there is still no response to conservative treatment in a noncoalescing mastoid, cortical mastoidectomy is recommended. Mastoidectomy is
performed immediately if there is radiological evidence of coalescing mastoiditis.
The aim of mastoidectomy is to debride necrotic tissue, improve ventilation of the
mastoid bone and prevent further intracranial complications [17].
21.2.2 Facial Nerve Paralysis
One of the complications of acute or chronic middle ear infection is facial paralysis.
Facial palsy following AOM is usually seen in children, is sudden in onset and
resolves rapidly with appropriate treatment [18]. In COM, with or without cholesteatoma, paralysis occurs gradually and the prognosis is generally poor. The pathogenesis of paralysis occurs with neuropraxia due to exposure to toxins, compression
or edema. The complication usually spreads through dehiscence in the tympanic
part of the fallopian canal, where dehiscence is most common. It can develop within
1–2weeks of AOM.The pathogens causing facial paralysis are usually similar to
those causing acute otitis media. The virulence of the microorganism and the host’s
resistance are critical to the prognosis of the disease, and if the infection has crossed
the fallopian canal, the facial nerve may be affected by inammation. With the onset
of inammation, edema develops. The edema puts pressure on the facial nerve
trapped in the canal and nerve conduction stops, a condition called neuropraxia. On
the other hand, the accumulation of purulent material or directly invading bacteria
exposes the nerve to extraneural compression and neuritis develops. The arterial
21 Complications ofOtitis Media
427
blood supply to the compressed nerve is impaired and ischemia occurs. This leads
to anoxia and degeneration of the nerve [19].
Facial paralysis due to COM can have several causes (e.g., compression due to
oedema, direct bacterial inammation, osteitis, bony erosion, neurotoxic substances
from cholesteatoma). When facial paralysis develops in a patient with COM, the
presence of cholesteatoma is suspected. In subacute and chronic infections, facial
paralysis occurs as a result of erosion of the Fallopian canal due to infection or cholesteatoma when the nerve meets the infection [20]. Facial paralysis usually develops due to extraneural compression in the tympanic part, particularly in the
pyramidal eminence and cochleariform prominence regions. It develops as a result
of compression of the nerve between the cholesteatoma and these anatomical
structures.
Facial paralysis due to otitis media is diagnosed clinically. Computed tomography scans can be used to determine the degree of facial canal involvement and the
extent of the disease. Electrophysiological tests are helpful in determining the prognosis of long-term facial paralysis [21, 22]. The aim of treatment is to remove the
infection from the middle ear and mastoid as quickly as possible. Hospitalization,
myringotomy, and systemic antibiotic treatment are usually sufcient for facial
paralysis due to AOM.The antibiotic regimen may be modied according to the
culture obtained at myringotomy, and some authors recommend concomitant corticosteroid therapy. Mastoidectomy is indicated in patients who do not respond to
medical treatment, have subperiosteal abscesses, coalescent mastoiditis, and persistent discharge. The purpose of mastoidectomy is to remove infected bone and soft
tissue. If the infection has not spread to the tympanic and vertical parts of the facial
nerve, it is not necessary to open the nerve sheath (epineurium). However, if the
infection has affected the nerve sheath, diseased bone and soft tissue should be
removed from the epineurium. Opening the nerve sheath is controversial and there
is no evidence that it alters the healing process. If there is pus extending into the
Fallopian canal, the sheath can be opened, but this is controversial as it may create
a pathway for active infection to reach the nerve. Recovery from complete paralysis
may take a long time, but total decompression of the facial nerve is not indicated
unless progressive nerve degeneration is demonstrated by electroneuronography.
However, in complete paralysis with loss of electrical excitability, the facial nerve
should be decompressed from the rst elbow to the stylomastoid foramen [23].
In the treatment of facial paralysis due to COM, in addition to antibiotic therapy,
surgical exploration is an absolute emergency. Modied radical mastoidectomy is
usually performed to remove the cholesteatoma and explore the facial nerve.
Cholesteatoma can affect any part of the facial canal, but the tympanic part and the
second elbow are most commonly involved. In cholesteatoma cases, the matrix is
removed and the facial nerve is exposed. After the healthy bone proximal and distal
to the affected area has been reduced to eggshell thickness with a diamond tourniquet, it is removed and the epineurium exposed. The disease on the epineurium of
the decompressed nerve is removed by blunt dissection. If the cholesteatoma is not
invasive, it is not necessary to open the nerve sheath. If there is invasive granulation
tissue in the bony canal, the canal should be opened at least to the extent of the
428
S. Şerier et al.
granulation tissue. Care should be taken not to open the nerve sheath unless indicated. As the perineurium is a strong barrier, it is very common for the nerve to be
exposed to infection if it is opened [20].
21.2.3 Labyrinthitis
There are several ways in which the labyrinth, or inner ear, can be affected by
insults. Both Inammation of the meninges or cerebrospinal uid (CSF) can enter
the inner ear via the cochlear aqueduct or internal auditory canal (IAC). Bacterial
meningitis can cause labyrinthitis and then, signicant hearing loss. Conversely,
infection can spread from the labyrinth to the central nervous system. Infection in
the middle ear, can also enter the labyrinth through the round or oval window and
cause injury. This is thought to be the mechanism behind the cases of labyrinthitis
observed in a study. In some rare cases, bacteria from a systemic infection can reach
the labyrinth via the bloodstream, following an unusual pattern of hematogenous
spread [24].
Labyrinthitis can be classied as either suppurative or serous. Suppurative labyrinthitis occurs when microorganisms, typically bacteria, invade the labyrinth and
cause damage to the cochlea and vestibular system (Fig.21.2). This form of labyrin-
thitis often results in permanent severe or profound hearing loss. Serous labyrinthitis occurs when the labyrinth is affected by toxic by-products of bacteria or
inammatory particles. With serous labyrinthitis, hearing problems are usually
milder and temporary. Typically, suppurative labyrinthitis has an initial serous phase
that precedes the purulent stage. However, it’s important to note that in meningococcal meningitis, labyrinthitis can begin directly with the purulent stage without a
preceding serous stage, with one notable exception [25]. Suppurative labyrinthitis
can lead to a condition known as “dead ear,” which occurs when bacteria and
Fig. 21.2 Computed tomograhy images of suppurative labyrinthitis
21 Complications ofOtitis Media
429
inammatory cells cause destruction of the basilar membrane. This destructive process also causes extensive damage to the labyrinth, including the destruction of the
organ of Corti and the spiral ganglion. The diagnosis of labyrinthitis is primarily
based on a detailed medical history. It is important to remember that dizziness associated with a known ear condition may be indicative of labyrinthitis. Contrastenhanced MRI may be used to conrm the diagnosis. This imaging technique
provides additional information for the diagnosis of labyrinthitis [26].
Because of the different clinical course of serous and suppurative labyrinthitis, it
is important to distinguish between the two conditions. In serous labyrinthitis,
symptoms are usually mild and subtle. The patient may experience sensorineural
hearing loss, which may go unnoticed and is predominantly high frequency.
Vestibular symptoms may also be present. The sense of imbalance may manifest as
intermittent positional vertigo or spontaneous episodes of vertigo, suggesting the
possibility of endolymphatic hydrops. Diplacusis, a condition in which sounds are
perceived differently in each ear, is another cochlear symptom of labyrinthitis. Total
hearing loss is not usually seen and there is a potential for hearing recovery. Initially
there is an irritative nystagmus with a fast phase towards the affected ear, followed
by a (paralytic) nystagmus towards the healthy ear. In suppurative labyrinthitis, the
auditory and vestibular symptoms are severe and of rapid onset. There is a complete
loss of the cochleovestibular response, resulting in a profound absence of both auditory and vestibular function. Vestibular symptoms are particularly severe and may
persist for several days. Suppurative labyrinthitis and meningitis should be considered in patients with severe and worsening symptoms. Treatment of labyrinthitis
aims to treat the underlying cause. In cases where AOM is the cause, myringotomy
and antibacterial therapy are usually sufcient. However, if the cause is perilabyrinthine osteitis or cholesteatoma, it is necessary to remove the affected tissue by mastoidectomy after administration of parenteral antibiotics. Some experts recommend
delaying surgery until the acute symptoms have resolved to prevent the spread of
infection. Once labyrinthitis has been diagnosed, appropriate antibiotic therapy is
started and symptom-relieving treatments are given. If symptoms do not improve,
the possibility of meningitis should be considered. If there is evidence of meningitis, a lumbar puncture should be performed to conrm the diagnosis. It is important
to note that suppurative labyrinthitis may resolve if the appropriate treatment for
meningitis is given [27].
21.2.4 Labyrinthine Fistula
A labyrinthine stula is observed in approximately 5–10% of cases of COM associated with cholesteatoma. Most commonly, the lateral semicircular canal is affected
[28]. In the majority of cases, stula development occurs due to bone erosion caused
by the presence of cholesteatoma. Erosion of the otic capsule can occur by two
mechanisms: either active mediators or compression by the cholesteatoma lead to
osteolysis, or inammatory mediators cause resorption of the otic capsule, as seen
in cases of COM without cholesteatoma but with granulation tissue [29].