Odontogenic Sinusitis: Classification, Etiology, Clinical Presentation, Diagnosis, and Treatment
A detailed overview of odontogenic maxillary sinusitis: causes, symptoms of acute and chronic inflammation, diagnosis, and modern treatment approaches.
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Injuries of the middle and inner ear are anatomical and functional damage to the structures of the middle and/or inner ear caused by a pathological force and resulting in hearing loss or vestibular disorders. A common cause of these conditions is mechanical, acoustic, or pressure-related trauma. The pathological process may involve the tympanic membrane, ossicular chain, oval and round windows, bony labyrinth capsule, and temporal bone. Clinically, these injuries manifest as conductive, sensorineural, or mixed hearing loss, tinnitus, and vestibular disturbances.
Main types of middle and inner ear injuries:
The following types of injuries are classified as middle ear injuries:
Inner ear injuries include:
Other injuries include posttraumatic mastoiditis.
All middle and inner ear injuries occur as a result of exposure to an external pathological factor. The most common causes are motor vehicle accidents, as well as injuries caused by the use of inappropriate objects for cleaning the ear canal or by foreign body penetration. Tympanic membrane perforation and ossicular chain injury may result from a sudden changes in pressure within the ear canal — known as barotrauma (a blow to the ear, a kiss, rapid submersion underwater, or rapid ascent), as well as from the head striking hard objects. Cases of ossicular chain dislocation during middle ear surgery or paracentesis are extremely rare.
Hemotympanum may be triggered by severe coughing or sneezing due to rupture of small blood vessels in the mucosa of the tympanic cavity. This condition can also occur after posterior nasopharyngeal tamponade for massive bleeding or adenotomy. In addition, hemotympanum may be a manifestation of a temporal bone petrous portion fracture.
Temporal bone fractures are a specific type of skull base fracture. In addition to road traffic accidents, the leading cause is fights, beatings. Longitudinal fractures occur when force is applied to the temporal region on the affected side, whereas transverse fractures occur with mechanical impact to the frontal or occipital region. It should be noted that all the mentioned types of injuries may occur in combination.
If diagnosis is insufficient or delayed, or adequate treatment is not provided in the presence of the above conditions, posttraumatic mastoiditis may develop. This occurs due to the introduction of pathogenic microflora from the nasopharynx or through a perforated tympanic membrane.
Traumatic perforation of the tympanic membrane is characterized by disruption of the integrity of all of its layers: epithelial, fibrous, and mucosal. A hole is formed at the site of the lesion, along the edges of which hemorrhagic drips are determined, and blood is found in the external auditory canal. In cases of temporal bone injury, leakage of cerebrospinal fluid (otoliquorrea) may also be observed.
The location and size of the perforation are important to select the appropriate patient management strategy.
Based on location, perforations are classified as:


Even with small tympanic membrane injuries, ossicular dislocations may occur. Traumatic perforation in the posterosuperior quadrant is frequently associated with disruption of the ossicular chain.
In hemotympanum, the tympanic membrane remains intact, while hemorrhagic fluid accumulates within the tympanic cavity. Consequently, the tympanic membrane may appear cyanopurplish and even protrude into the auditory canal lumen.
Sources of hemorrhage:
Disruptions of the ossicular joints occur more frequently than fractures and may develop either in combination with traumatic perforation of the tympanic membrane or independently.
The most common ossicular chain injuries:
The incus is the heaviest of the three middle ear ossicles and is supported by two weak ligaments; therefore, it is more commonly subject to dislocation and fracture than the other ossicles.
The malleus is maximally protected from injury and dislocation due to its fixation to the tympanic membrane, the tensor tympani muscle, and the presence of three ligaments (anterior, posterior, and superior).
Ossicular fractures are rare and may occur at any location. The most common are fractures of the long process of the incus and fractures of the stapes crura. Fracture of the malleus handle has also been described in isolated cases. In fractures, displacement of the intact ossicular chain occurs toward the sites of ligament attachment.
Fractures of the petrous portion of the temporal bone are classified according to the axis of injury:
Combined fractures are also encountered in clinical practice.
Posttraumatic mastoiditis is an inflammatory condition developing against the background of traumatic changes in the middle ear, most commonly in the presence of pathological contents (blood) within the mastoid air cells. The inflammatory process spreads to the mucous membrane and bone tissue of the tympanic cavity and temporal bone.
As the condition progresses, bone caries develops with formation of sequestra surrounded by purulent contents. In the presence of perforation in the tympanic membrane is determined by the oozing of pus into the external ear canal. The tympanic membrane may remain intact, but its bulging is observed, and the identifying signs are smoothed. The posterior wall of the ear canal may also be overhanging.
General symptoms of middle and inner ear injuries:
The type of hearing loss depends on the type of injury: conductive hearing loss is characteristic of tympanic membrane and middle ear injuries, whereas sensorineural or mixed hearing loss is observed with inner ear involvement.
Features of the clinical presentation in various injuries:
In both types of temporal bone fractures, Battle’s sign may be present — postauricular hematomas. Fractures of the temporal bone are also associated with early and late complications, the most serious of which include damaged carotid artery, facial nerve damage, mastoiditis, and meningitis.
Diagnosis is based on findings from an otolaryngologic examination and a carefully collected medical history. An important stage of diagnosis is otomicroscopy.
Vestibular function must be assessed; audiometry, tympanometry, tuning fork tests, and vestibular tests are performed, as well as hearing assessment using whispered and conversational speech.
Among instrumental diagnostic methods, computed tomography (CT) of the temporal bones with thin sections is mandatory to determine the extent of injury. In some cases, consultation with a neurologist, neurosurgeon and ophthalmologist is recommended. Electroneuromyography is used to assess facial nerve function.
For tympanic membrane perforations, a watchful waiting approach is the most justified, since even large perforations are capable of spontaneous closure. If the perforation is suspected to have been infected at the time of injury, topical antibacterial medications in the form of ear drops are prescribed. An important condition for optimal healing is prevention of secondary infection, including restricting water entry into the external auditory canal and ensuring proper function of the Eustachian tube.
If healing does not occur within 2–3 months, as well as in cases where the perforation is located in the flaccid portion of the tympanic membrane or extends to the tympanic annulus, myringoplasty is performed. When the tympanic membrane is infected, either systemic or local antibacterial drugs are prescribed. After myringoplasty, follow-up with an ENT physician is recommended for at least 2 years, because the risk of cholesteatoma formation remains.
In case of hemotympanum, oral antibacterial therapy and topical nasal medications (nasal decongestants) are prescribed to improve Eustachian tube function; autoinsufflation of the Eustachian tube is also recommended. With a favorable outcome, the blood undergoes lysis within 7–10 days.
If the contents of the tympanic cavity become infected, puncture of the cavity is performed, pathological discharge is aspirated, and bacteriological examination is carried out. Antibacterial therapy is prescribed according to the results of susceptibility testing.
To restore the ossicular chain, revision of the tympanic cavity and tympanoplasty are performed 3–6 months after the injury. This delay is intentional, as spontaneous hearing improvement may occur during this period when scar tissue bridges the ruptures.
Conservative therapy includes the use of systemic corticosteroids to prevent delayed facial nerve paresis and systemic antibacterial therapy to prevent bacterial complications. Regarding surgical treatment, a watchful waiting approach is considered appropriate.
Early surgical intervention is necessary in the following cases:
If facial nerve edema develops during the delayed period despite conservative therapy, decompression of the facial nerve canal is performed. In case of continued liquorrhea for more than 14 days, surgical treatment with closure of the defect is also indicated.
For inflammatory complications (mastoiditis, meningitis), antromastoidotomy with revision of the tympanic cavity and mastoid air cells is performed, and broad-spectrum antibacterial medications are prescribed.
1. How can you determine that the inner ear has been damaged?
2. What should first aid involve for injuries to the middle and inner ear?
3. When is surgical intervention required for ear injuries?
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