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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4507_Библиотеки_им_академика_М_И_Перельмана.pdf
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S. Şerier et al.
Disagreement in the management of labyrinth stula is often due to the lack of a
universally accepted staging system for this condition. However, two commonly
used and closely related classications are worth mentioning. (Tables 21.2,21.3)
These classications provide a framework for assessing and categorizing labyrinth
stula, aiding management decisions and facilitating communication between
healthcare professionals [30, 31].
Patients with a labyrinth stula often present with recurrent episodes of vertigo.
They may also have additional signs and symptoms associated with cholesteatoma.
Approximately 60% of patients with vertigo and imbalance are found to have a stula. Patients with a labyrinthine stula may experience sudden vertigo when
exposed to loud noises, known as the Tulio phenomenon. If a patient presents with
dizziness and has a known or suspected COM with cholesteatoma, it is recommended that a stula test and CT scan be performed to assess for the presence of a
labyrinthine stula [32]. During the stula test, positive or negative pressure is
applied to the external auditory canal using a pneumatic otoscope or manual pressure on the tragus cartilage to elicit a response. The pressure applied during the test
is transmitted to the middle ear and mastoid air cells. This creates positive and negative pressures that cause movement of the endolymph in the lateral canal. These
movements, known as ampullopedal and ampullofugal ows respectively, lead to
the occurrence of vertigo and nystagmus. In the presence of a stula, nystagmus is
observed with a rapid eye movement towards the affected ear when positive pressure is applied and towards the unaffected ear when negative pressure is applied.
The nystagmus is typically horizontal as most stulas occur in the lateral semicircular canal. However, if the posterior or superior canals are involved, vertical or vertical-rotatory nystagmus may be observed. It’s important to note that the stula test
can only give a positive response if vestibular function is intact. In cases where there
is a localized loss of function in the ampulla of the affected duct or a generalized
loss of labyrinth response, a false negative result may occur. Therefore, a negative
stula test result does not completely rule out the presence of a stula. The stula
test may give false positive results in cases of Meniere’s disease, superior semicircular canal dehiscence, hypermobile stapes, and autosyphilis. It is important to
remember that even if no stula is found in patients with cholesteatoma, there is still
a possibility that a stula may be found during surgery. In other words, not all cases
of stula are necessarily symptomatic [33].
Table 21.2 The
classication of labyrinthine
stulas proposed by
Dornhoffer and Milewski
Type I Bone erosion with intact endosteum
Type IIa Endosteum is damaged, but the
perilymphatic system remains protected
Type IIb Perilymphatic system is damaged or
accidentally aspirated
Type III Membranous labyrinth and endolymph are
damaged
Adapted from Ref. [30]
21 Complications ofOtitis Media
Table 21.3 Palva and Ramsey classication of labyrinthine Fistulas
Stage I “Blue line” visible at the top of the canal, with thin bone
Stage IIAll bone is absorbed, but the endosteum remains intact
431
Stage
III
Stage IVExtensive bone erosion with invasion of the choleste
Adapted from Ref. [31]
True stula, with the perilymphatic space open and cholesteatoma directly contacting
the membranous semicircular canal
Although the denitive diagnosis of a stula is usually made during surgery, it is
recommended that high-resolution CT scans be used for preoperative detection.
Fistula treatment is inuenced by several factors, including the location and size of
the stula, the experience of the surgeon and the hearing status of the patient. Even
experienced surgeons face the risk of inner ear damage and possible hearing loss. In
the presence of a cholesteatoma, a tympanomastoidectomy is usually performed
[32, 34]. The decision to perform a canal wall down or canal wall up procedure is at
the surgeon’s discretion. During surgery, the cholesteatoma matrix in the area of the
stula is carefully opened and dissected over the endosteum. For stulas smaller
than 2mm, the matrix is carefully dissected away from the endosteum and removed.
Materials such as fascia, perichondrium or bone are used to repair the stula.
However, if the endosteum is accidentally torn during dissection, the cholesteatoma
matrix is left in place and the operation is terminated. In the case of larger stulas,
where the endosteum is open but there is no invasion of the perilymphatic space,
efforts are made to remove it safely. The defect can be repaired with materials such
as fascia and bone. However, if there is an invasion of the perilymphatic space, several options may be considered. One option is to remove the cholesteatoma matrix
and close the defect with soft tissue and bone. Another option is to perform a canal
wall-down procedure, leaving the matrix as part of the cavity. Alternatively, a canal
wall-up procedure can be performed, leaving the matrix in place to be removed in a
subsequent operation [35].
21.2.5 Petrositis
Petrositis, also known as “petrous apicitis,” refers to inammation of the petrous
part of the temporal bone. This condition is considered a rare complication of otitis
media due to the limited pneumatization of the petrous bones, but it carries a high
morbidity [36]. The petrous apex cells are divided into two groups, anterior and
posterior, by a coronal plane passing through the internal acoustic canal. The cells
of the posterior group arise from the epitympanum and antrum, surround the semicircular canals, extend towards the base of the petrous pyramid and often reach the
apex. The cells of the anterior group are found in part of the temporal bones, surrounding the tympanum, hypotympanum and Eustachian tube, and reaching the
apex of the pyramid around the cochlea. Below the anterior cell group is the carotid
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S. Şerier et al.
artery and above it is Meckel’s cave, making surgical access to this area challenging. Inammation of the petrous air cells has similarities to that of the mastoid
system [37].
Petrositis occurs mainly at the apex of the petrous bone and is considered a form
of mastoiditis. It develops when the mastoid infection spreads directly to the petrous
apex. While mastoid disease usually responds to medical and/or surgical treatment,
apical disease tends to persist. In cases where no bone changes are seen in the cell
walls, petrositis may not be diagnosed, but petrous involvement may still be considered. However, if there is bone involvement, petrositis is diagnosed. The dangerous
and high morbidity of petrositis is due to the limited drainage and proximity to
intracranial structures. The symptoms of petrositis are related to the innervation of
air cells and structures adjacent to the apex. Symptoms of petrositis can sometimes
be subtle or mimic middle ear and mastoid infections. The two most common symptoms are deep retroorbital pain and otorrhea. Increased pressure in the mastoid air
cells causes pain in the mastoid region and ear, while increased pressure in the
petrous apex often causes pain that is reected in the retroorbital region. Retroorbital
pain is caused by inammation of the trigeminal ganglia. Pain associated with petrositis is attributed to the affected region of the petrous pyramid. In posterior petrositis, patients may experience occipital, parietal, or temporal pain, while anterior
petrositis may cause pain in the frontal or retro-orbital region. Involvement of the
petrous apex can lead to sixth cranial nerve palsy, resulting in diplopia (double
vision). The sixth nerve (abducens) passes through the Dorello canal under the petroclinoid ligament (Gruber’s ligament), making it susceptible to compression by
edema. The triad of symptoms of diplopia, retrobulbar pain, and persistent otorrhea
due to abducens palsy, is known as “Gradenigo syndrome.” Petrositis can also lead
to cranial nerve palsies involving the 7th (facial) and 8th (vestibulocochlear) cranial
nerves. Petrositis should be considered in patients who have undergone radical mastoidectomy and have experienced persistent purulent discharge and pain, and the
diagnosis can be conrmed by high-resolution CT [38, 39].
The main treatment for petrositis is antibiotics, as the area is difcult to access
by surgery and antibiotics generally show a positive response. The effectiveness of
treatment can be monitored by monitoring infection parameters. In cases of abscess
formation, resistance to medical treatment, or petrous bone necrosis, surgery is
required. The aim of surgery is to drain the abscess without damaging important
anatomical structures such as the facial nerve and labyrinth. After completion of
antibiotic therapy, surgical mastoidectomy is usually the preferred treatment. In
more refractory cases, additional measures may be required. This may include
opening all the labyrinthine cells around the labyrinth to facilitate drainage. The
choice of surgical approach depends on factors such as the patient’s hearing, the
pneumatization of the temporal bone and the location of the infection. If the patient
has no hearing, the translabyrinthine or transcochlear approach is usually chosen. In
patients with hearing, the infracochlear approach is used for drainage. In situations
with advanced complications such as abscess and osteitis, or when the temporal
bone is poorly pneumatized, the middle fossa approach is used [38–40].
21 Complications ofOtitis Media
433
21.3 Intracranial Complications
21.3.1 Meningitis
Although the incidence of complications from otitis media has decreased signicantly
due to the timely and effective use of antibiotics, serious complications can still occur.
The most common intracranial complication of otitis media in children is meningitis,
which typically develops after AOM, whereas in adults it is more common after
chronic otitis. Meningitis due to otitis media can occur by various routes, including
hematogenous spread, direct invasion through bone erosion, preformed tracts in the
middle ear and mastoid, penetration through the oval and round windows, retrograde
thrombophlebitis, skull base fractures after trauma, or CSF leakage [41, 42].
The most common causes of purulent meningitis in adults vary according to age
and the individual’s immune system, but H. inuenzae, Neisseria meningitidis and
S. pneumoniae are often involved. These are responsible for about two-thirds of all
cases of bacterial meningitis [43].
Meningitis is a clinical condition characterized by symptoms such as fever, headache, altered consciousness, weakness, nausea, and vomiting caused by inammation of the membranes surrounding the brain. On examination, neck stiffness,
Kernig’s sign, Brudzinski’s sign, epileptic seizures, cranial nerve palsies and focal
neurological decits may be observed. Usually, abducens nerve palsy tends to
improve with treatment of the meningitis, whereas eighth nerve palsy following
meningitis often leads to permanent hearing loss [38].
If meningitis is clinically suspected, immediate initiation of antibiotic treatment is
essential. Intravenous administration of third-generation cephalosporins, especially
those capable of crossing the blood-brain barrier, is preferred. CT scan is performed
to exclude other intracranial complications such as brain abscess or mass. If there are
no contraindications, a lumbar puncture (LP) is performed to conrm the diagnosis
and to obtain a culture for analysis. Meningitis associated with increased intracranial
pressure results in elevated CSF (>200 mm-H2O) and a cloudy appearance. In
untreated cases, the CSF typically contains 1000–10,000 leukocytes per mm3, of
which 85–95% are neutrophils in the early stages. In addition, acute bacterial meningitis is often characterized by high CSF protein levels (usually 100–500mg/dl) and
low glucose levels (less than 40% of blood glucose or<40mg/dl). The most effective
antibiotic treatment is then given based on the pathogen identied in the culture result.
In addition, an otoscopic examination should be performed to exclude otological
causes, and high-resolution CT imaging may be requested to assess the condition of
the temporal bone and surrounding structures, including any congenital malformations that may contribute to meningitis. MRI may provide a more detailed view of the
meninges and the inammatory state of the brain [38].
In cases of meningitis due to AOM, the primary approach to treatment is medical, with the exception of myringotomy. Myringotomy involves drainage of purulent material and culture and susceptibility testing. If coalescent mastoiditis persists
despite maximal medical treatment, mastoidectomy is considered. Meningitis due
to COM or cholesteatoma is considered a surgical and medical emergency due to
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S. Şerier et al.
the potential risk of dural dehiscence and passage of purulent material into the subarachnoid space (Fig. 21.3). The surgical goal is to completely and meticulously
remove the disease from the ear and ensure proper drainage. The entire affected
dura is exposed and excess granulation tissue is removed. Abscesses on either side
of the dura are drained. When draining an extradural abscess, it is important to identify the dural defect, which can then be repaired by placing intradural and extradural
fascia. Although postoperative CSF leakage may occur, improvement is expected as
the meningitis resolves and excessive CSF production normalizes [44].
21.3.2 Lateral Sinus Thrombosis
Infections and inammations in the middle ear and mastoid can lead to thrombosis
and thrombophlebitis in the dural sinuses due to their close proximity. The infectious process may spread from the ear and mastoid region to the sinuses, causing
these complications. In the current era of antibiotic treatment of suppurative ear
disease, lateral sinus thrombosis (LST) is observed in approximately 6% of all intracranial complications. The LST is one of the most common complications of the
COM.In the pre-antibiotic era, it was the second most common and life-threatening
complication of otitis media, just behind meningitis [45]. Inammation in the mastoid cavity can spread by two main routes: direct invasion, where cholesteatoma
Fig. 21.3 Algorithm of treatment for meningitis associated with otitis media
21 Complications ofOtitis Media
435
inltrates the sinuses or causes bone erosion, and thrombophlebitis of the mastoid
emissary vessels. Thrombophlebitis is typically caused by vascular damage due to
inammation, leading to thrombus formation. If the thrombus breaks off and enters
the bloodstream, it can facilitate the spread of infection, leading to metastatic
abscesses. As the thrombus enlarges, it may involve the sagittal sinus or the internal
jugular vein. Involvement of the internal jugular vein increases the risk of pulmonary embolism and may even lead to sepsis if it reaches the right atrium. Intracranial
dissemination may lead to brain abscess formation, while involvement of the sinus
junction may cause otitic hydrocephalus [46, 47].
The clinical presentation of LST secondary to COM is highly variable, making a
precise denition difcult. Patients may present with a variety of symptoms, and the
presence of comorbidities or previous treatment prior to admission further complicates the picture. For some patients, LST may be life-threatening with severe sepsis
at the time of diagnosis, while others may have relatively mild or no symptoms and
the condition may only be detected on imaging studies. The most common symptoms and signs associated with LST are severe headache, ear pain (otalgia), picket
fence fever, and papilledema. These are considered to be specic indicators of
LST.Since the introduction of antibiotics, the incidence of “picket fence” fever, a
characteristic symptom of lateral sinus thrombosis, has decreased. When the sinus
lumen is blocked and cortical venous circulation is interrupted, symptoms such as
headache, papilledema, and increased intracranial pressure occur. Tenderness and
swelling over the mastoid area (known as Griesinger’s sign) are characteristic signs
of lateral sinus thrombosis, as this is a reex thrombosis of the mastoid emissary
vein. The increased pressure in the region due to the occlusion of the jugular bulb
can lead to paralysis of the ninth, 10th, and 11th cranial nerves [38, 45].
The denitive diagnosis of LST is usually made using CT and MRI scans. If
patients have a sudden onset of fever and signs of increased intracranial pressure, a
CT scan is usually ordered to investigate the possibility of LST.The CT scan may
show a delta sign, which is a contrast-enhancing area on the sinus wall. However,
this is not always present. MRI is considered more effective than CT in detecting
thrombi because it shows increased signal within the lumen of the thrombus. MRI
is the preferred method for diagnosing LST and, together with CT, can help to detect
the presence of intracranial complications. Magnetic resonance venography is a
reliable method for diagnosing LST, as it shows the absence of blood ow and signal loss in the sinus. This imaging technique can be used to monitor the thrombus
with serial scans in the case of a large thrombus [45].
Treatment for LST includes intravenous broad-spectrum antibiotics and surgery
to remove the source of the infection. Research has shown that myringotomy and
antibiotic treatment are effective for LST that develops after AOM.Some studies
have shown that the sinus can be re-canalized without mastoidectomy. However, in
cases of septic thrombus, septic embolism, or sinus abscess, mastoidectomy is necessary to remove infected thrombus or pus through sinus exploration. Adequate
bleeding from both ends of the incised sinus is desirable during the procedure. In
cases where LST is associated with autistic hydrocephalus, treatment includes the
use of corticosteroids, mannitol, and uid restriction to reduce intracranial pressure.
If the pressure remains high despite these measures, serial lumbar punctures may be
attempted to reduce the pressure. If LST is secondary to COM, with or without
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S. Şerier et al.
cholesteatoma, surgery is required in addition to antibiotic therapy. During mastoidectomy, cholesteatoma and granulation tissue are removed. The sinus wall is then
thinned to reach the sinus and any abscess or thrombus is drained from the sinus. If
the sinus is accessible and palpable, drainage can be achieved by aspiration. Blood
aspiration usually does not require further surgery. However, if the sinus is immobile and non-palpable and aspiration is not possible, the sinus wall may be opened.
It is important to note that there are conicting opinions about this approach, as
some studies suggest that after treatment the infection around the sinus may recanalize on its own without surgery. Antibiotic therapy should be continued for at least
two weeks after surgery. The use of anticoagulants to treat LST remains controversial. Some experts believe that anticoagulants may lead to an increased risk of septic
embolism due to thrombus dissolution. On the other hand, some experts choose to
use anticoagulants to prevent further growth of the thrombus. The decision to use
anticoagulant therapy should be carefully considered. If medical treatment fails to
relieve the symptoms of increased intracranial pressure, the use of anticoagulants
may be considered [45, 48].
21.3.3 Brain Abscess
A brain abscess is a localized infection with pus formation in the brain tissue. It is
more common in children and adults in their forties. Men are more affected than
women. Although brain abscesses used to be more common, their incidence has
decreased with the advent of antibiotics. About 15–25% of all brain abscesses are
associated with otitis media [49]. Among the complications of otitis media, brain
abscess is the most life-threatening. Unlike meningitis, which is usually associated
with AOM, most brain abscesses result from COM, with cholesteatoma being the
primary cause. A variety of microorganisms are responsible for the formation of
brain abscesses, with anaerobes being detected at high rates in polymicrobial cultures. Aerobic gram-positive cocci and gram-negative bacilli may also be present,
with streptococci, staphylococci and proteus being the most common [50].
Brain abscesses can develop in three ways: (1) as a result of infection in the
immediate environment, such as otitis media; (2) from a distant source of infection,
such as chronic pyogenic lung disease; or (3) following head trauma or cranial surgery. The primary mechanism of autogenic brain abscess is not a direct extension
from the dura but rather hematogenous spread, often associated with retrograde
venous thrombophlebitis. The temporal lobe and cerebellum are the most commonly affected regions. Temporal lobe abscesses are usually due to spread through
the tegmen tympani, while cerebellar abscesses are often associated with suppurative labyrinthitis and/or lateral sinus thrombophlebitis. Although the dura is highly
resistant to infection, persistent infection, osteitis, or granulation tissue may cause
localized inammation of the dura, leading to retrograde thrombophlebitis of the
dural vessels which may terminate in the adjacent white matter. Infection progressing to small terminal veins in the white matter may lead to encephalitis. In this
region, the defence against infection is minimal and localized encephalitis rapidly
21 Complications ofOtitis Media
437
progresses to necrosis and liquefaction in the brain tissue (focal suppuration).
Edema develops around this necrosis and liquefaction. In about two weeks, an
abscess capsule forms surrounded by granulation tissue, which forms as a result of
the broblast response to inammation (Fig.21.4) [38, 51].
As the abscess enlarges, it may extend into the ventricles, leading to increased
intracranial pressure. In some cases, weakness of the capsule and softening of the
surrounding tissue may allow the infection to progress towards the ventricles or
cortex, resulting in drainage of the abscess into the ventricles or subarachnoid space
[52]. Cerebellar abscesses occur in the conned space of the posterior fossa, adjacent to the brainstem. Therefore, cerebellar abscesses cause earlier symptoms and
more severe outcomes than temporal abscesses. If left untreated, temporal lobe
abscesses can spread to the ventricular or subarachnoid spaces, leading to fatal
meningitis.
Clinically, headache, high fever and focal neurological decits are common in
patients with brain abscess. They may also have a toxic appearance and drowsiness.
The focal decits vary according to the location of the abscess. Seizures may be
seen in temporal lobe abscesses. Brain abscesses are typically divided into four
stages, including early cerebritis, late cerebritis, early capsule formation and late
capsule formation which is the ruptured phase and drains into the ventricles [38].
Fig. 21.4 Brain abscess
formation associated with
otitis media
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S. Şerier et al.
In patients with suspected intracranial involvement, it is important to start antibiotic treatment immediately, followed by radiological imaging. MRI is considered
the superior imaging modality for detecting brain abscesses. However, CT scans are
more effective in identifying the underlying cause of the abscess and showing any
bone erosion in the mastoid and middle ear. The use of serial contrast-enhanced CT
scans can help monitor the effectiveness of treatment over time. As with meningitis,
intravenous antibiotics must be given promptly to patients diagnosed with brain
abscesses [53].
Once the patient’s neurological condition has stabilized, surgical intervention is
essential. Surgical approaches to brain abscess include aspiration, open drainage,
and exploration. Aspiration is appropriate for patients who respond well to medical
therapy, those with multiple abscesses, and those with concomitant meningitis.
Myringotomy and aspiration may be sufcient for brain abscesses due to
AOM.However, mastoidectomy is performed for COM with or without cholesteatoma. The timing of mastoidectomy may vary based on different opinions, but it is
usually performed when the patient’s condition has stabilized after neurosurgical
treatment [38].
21.3.4 Otitic Hydrocephalus
Otitis media-associated otitic hydrocephalus is a rare complication. It is characterized by increased CSF pressure with normal CSF biochemistry [54]. There are no
focal neurological abnormalities other than those associated with increased intracranial pressure. The specic causes or mechanisms that lead to this rare condition
are still unknown and not fully understood. Some theories suggest that it may be
related to either overproduction or impaired absorption of CSF.Other hypotheses
include dysfunction of the arachnoid villi due to sinus thrombosis or localized meningitis. Cerebral edema and venous circulation disorders have also been considered
as potential mechanisms [38].
Clinically, the disease is characterized by bilateral papilledema (swelling of the
optic discs) and paralysis of the sixth cranial nerve on the affected side. These clinical features are important indicators of the disease. A lumbar puncture will show
increased CSF pressure while CSF biochemistry remains within normal limits,
which is a hallmark of otitic hydrocephalus. MRI may be helpful in assessing ventricular enlargement and detecting associated intracranial complications such as
sigmoid sinus thrombosis. However, a diagnosis of autistic hydrocephalus can be
made on the basis of clinical symptoms, papilledema and increased intracranial
pressure even in the absence of ventricular dilatation or meningitis [55].
The primary goals of treatment are to reduce intracranial pressure, treat any earrelated problems, and prevent the potentially serious complications of optic nerve
damage. In cases of dural thrombosis, mastoidectomy is necessary and it is essential
to reduce intracranial pressure, in addition to antibiotic and surgical treatment. At
the same time, close monitoring for vision loss and herniation is of paramount
importance. Reduction of CSF pressure can be achieved by the use of steroids,
21 Complications ofOtitis Media
439
diuretics, and uid restriction, while the combination of furosemide and mannitol
may have a synergistic effect in reducing pressure. If pressure remains elevated
despite treatment, serial lumbar punctures are recommended but must be performed
with caution to avoid herniation. In patients with visual loss, the option of a lumboperitoneal shunt may be considered, and in certain situations, optic nerve decompression may be required [55, 56].
21.3.5 Epidural Abscess
The epidural space is a potential area between the bone and the dura. Although
abscess formation in this space is rare, it can be a precursor to thrombophlebitis or
brain abscess. It typically develops as a complication of COM with cholesteatoma.
The cholesteatoma causes erosion of the bone tissue and may extend to the dura. If
the infection persists, pus accumulates in this area, leading to the formation of an
epidural abscess. Epidural abscesses usually cause no symptoms unless they become
quite large. They are often discovered during cholesteatoma surgery when pus is
found, or incidentally on tomography. Common symptoms include headache and
ear pain due to irritation of the dura. In patients with COM, the presence of an
abscess may be suspected if headache and ear pain do not improve, which may
indicate an intracranial complication [57].
Drainage and antibiotics are needed to treat an epidural abscess. A mastoidectomy is performed to drain the abscess. This involves carefully examining the
affected areas, such as the tegmen and posterior fossa, and removing pus and granulation tissue. Great care is taken to avoid damaging the dura. Antibiotic treatment is
continued until symptoms and signs improve [58].
21.3.6 Subdural Empyema
Subdural empyema, an extremely rare complication of middle ear infection, is the
accumulation of pus between the dura and the arachnoid mater. It is called an
“empyema” because of the presence of pus in a specic anatomical cavity. Unlike
an abscess, where pus forms in a capsule, subdural empyema occurs when pus
spreads into the subdural space, potentially causing a mass effect. Sudden and
severe headache is a common symptom of subdural empyema. This condition can
put pressure on the cerebral cortex, leading to focal neurological decits and seizures. It is important to avoid lumbar puncture in cases of subdural empyema to
prevent herniation. MRI is a more sensitive diagnostic tool for differentiating
between epidural and subdural infections (Fig.21.5) [59].
Subdural empyema requires immediate surgical intervention, as early treatment
leads to better outcomes. In addition to surgery, the patient may be given corticosteroids, antibiotics, and anticonvulsants if seizures are present. Emergency drainage is
a critical step to remove the pus, and this is achieved through a craniotomy performed by a neurosurgeon [38]. Once the patient’s condition has stabilized,