Diseases of the ear can cause complications as a result of the disease process and are classified into either intracranial or extra cranial complications.

Extracranial complications

Hearing loss-perforation
Facial paralysis
Larbinthine fistula
Acute petrositis
Subperiosteal abscess

Intracranial complications

CSF Otorrhea
Brain abscess
Extradural abscess
Subdural abscess
lateral sinus thrombosis

Hearing Loss-perforations

Tympanic membrane perforation is a well-known complication of untreated otitis media. It can develop in the setting of either acute or chronic ear disease. The common pathogenic pathway is excessive pressure on the TM, either from pressurized purulent matter in the middle ear or from long-standing eustachian tube dysfunction and its associated atelectasis. The resulting defect usually occurs in the pars tensa and can vary considerably in size, depending on the virulence of the organism.

Although most TM perforations heal spontaneously, some patients are left with a persistent hole in the eardrum. A patient with a chronic perforation classically presents with a mild conductive hearing loss with or without otorrhea. Hearing loss associated with a TM perforation can range from 0 to 40 dB, varying also with the status of the ossicular chain. Direct visualization of the defect is best performed with the otomicroscope. Careful binocular examination is important for ruling out occult cholesteatoma or potential ossicular pathology.

The results of tympanoplasty for chronic TM perforations are excellent in experienced hands. Successful closure of the perforation and improvement in hearing are typically seen in greater than 90% of patients, even in the face of nonsuppurative otorrhea.


Mastoiditis is an infection in the mastoid cavity and may manifest in one of two ways: acute periostitis (spread of infection via venous channels resulting in inflammation of the periosteum) or acute osteitis (bony destruction of mastoid air cell trabeculae). The latter is often referred to as coalescent mastoiditis. Acute mastoiditis can develop from AOM despite prior antibiotic treatment.
The hallmark triad of symptoms of acute mastoiditis comprises (1) otalgia, (2) postauricular pain, and (3) fever. Otorrhea and hearing loss are less frequently reported. The most common presenting sign, postauricular tenderness, is seen in over 80% of cases.2 In addition, protrusion of the pinna and postauricular erythema and swelling are classic findings. Induration over the mastoid is thought to be a harbinger of impending subperiosteal abscess. Temporal bone computed tomographic (CT) scanning is the diagnostic study of choice to detect coalescent mastoiditis, which is characterized by a loss of bony trabeculae. The majority of cases of acute mastoiditis can be treated conservatively with intravenous antibiotics and myringotomy, with or without tympanostomy tube placement. Culture-directed antimicrobial therapy is paramount to the successful treatment of acute mastoiditis.Therefore, a culture should always be obtained. Mastoidectomy is required whenever there is significant bony destruction or a poor response to up to 2 weeks of conservative management. The goal of surgery is to debride necrotic bone and to prevent intracranial extension of infection.

Facial Paralysis

Prior to the advent of antibiotics, the prevalence of facial nerve paralysis in chronic otitis media (COM) was greater than 2%.3 More recent reports indicate that this complication is now exquisitely rare. Facial nerve paralysis within the first 10 days of AOM is believed to be caused by edema of the nerve within the fallopian canal, similar to Bells palsy. In these cases, complete recovery from facial paralysis may be expected with conservative treatment. On the other hand, facial paralysis seen beyond 2 weeks of infection should be assumed to be the result of erosion of the osseous facial canal with exposure of the nerve to advancing suppuration.

High-resolution temporal bone CT scanning is essential in the evaluation of facial nerve palsy associated with otitis media.

Treatment of facial nerve paralysis as a complication of otitis media requires the use of intravenous antibiotics and prompt surgical intervention. Surgery is indicated to arrest the coalescent process and to protect the nerve from partial destruction. The tympanic segment is the most common area of involvement, suggesting that the surgical procedure should, at a minimum, eradicate infection from the middle ear. For an incomplete paralysis associated with protracted AOM, intravenous antibiotics and wide-field myringotomy or tympanostomy tube placement may be adequate.Facial nerve decompression is infrequently indicated. However, for complete facial paralysis with loss of electrical excitability, facial nerve exploration from the first genu to the stylomastoid foramen should be accomplished.


Labyrinthitis is the most frequent intratemporal complication of otitis media, owing to extension of infection within the temporal bone. Similar to meningitis,labyrinthitis has two clinically distinguishable subtypes: (1) localized, circumscribed, or serous labyrinthitis without total and permanent loss of function and (2) diffuse purulent or suppurative labyrinthitis with permanent total destruction of the sensory elements within the labyrinth.
Serous labyrinthitis is almost always an extension by preformed or acquired pathways which include the annular ligament of the oval window, the round window membrane, and the cholesteatomatous fistula. The symptoms of serous labyrinthitis are the result of disturbed vestibular and cochlear function, nearly always with a depression of sensory response. The vestibular symptoms precede the cochlear symptoms by hours to days when the site of invasion is a semicircular canal. These symptoms typically consist of profound vertigo, nausea, and vomiting. Patients usually demonstrate spontaneous nystagmus toward the unaffected ear and some degree of ataxia with past-pointing. The cochlear symptoms of serous labyrinthitis consist of primarily high-frequency sensorineural hearing loss with distortion of hearing and diplacusis.
Treatment of the serous labyrinthine inflammation is directed toward the etiologic factor. If the cause is an early acute suppurative otitis media, myringotomy and antibacterial therapy will suffice. If the cause is perilabyrinthine osteitis or cholesteatoma, mastoidectomy with removal of diseased bone should be combined with parenteral antibiotics
Suppurative Labyrinthitis has the same etiologic factors and pathways of invasions to serous labrynthitis. An exception to this rule is involvement of the labyrinth secondary to generalized meningitis, in which case, purulent labyrinthitis usually occurs without a prodrome of serous labyrinthitis.
The symptoms of suppurative labyrinthitis are similar to those of serous labyrinthitis, including the lack of fever. However, there are some key differences. The symptoms of suppurative labyrinthitis are more rapid and intense, with gradual improvement over the ensuing days. Also, the onset of severe vestibular symptoms is accompanied by a complete loss of cochleo-vestibular response. Notably, the caloric response is conspicuously absent from the diseased ear. The most important treatment of suppurative labyrinthitis is close and continuous monitoring for symptoms of intracranial extension. Antibiotics should be administered, albeit more to aid in preventing the spread of infection than in the expectation that the drug will enter the infected labyrinth in therapeutic concentrations. If meningeal signs are noted, then a lumbar puncture should be performed immediately. Any evidence of intracranial spread warrants surgical labyrinthectomy.

Labyrinthine fistula

A fistula of the labyrinth may be surgically produced or may occur as a consequence of suppurative or neoplastic ear disease. The vast majority of cases of fistula, however, occur as a result of bone erosion by cholesteatoma. In fact, the development of a labyrinthine fistula is so characteristic of cholesteatoma that a thorough evaluation should be initiated even in the absence of typical findings such as granulation tissue and drainage.

Patients with labyrinthine fistulae most often present with episodic vertigo. However, differentiating between a labyrinthine fistula and other benign vestibular and non-vestibular disorders based on history alone can be difficult. Thus, the fistula test can be helpful in making this clinical distinction. It is easily performed using either pneumatic insufflation or manual tragal pressure to apply positive or negative pressure to the ear. Pressure perturbations of the soft tissue covering a fistula result in nystagmus (produced by the movement of endolymph toward or away from the ampulla) and vertigo. A positive test consists of a quick component of nystagmus toward the affected ear with the application of positive pressure. As the vast majority of fistulae occur in the lateral semicircular canal, the nystagmus is most frequently horizontal. Conversely, the nystagmus is vertical with a fistula of either vertical canal. With a large (> 2 mm), far-anterior fistula, which exposes simultaneously the ampullae of the horizontal and superior canals, the nystagmus is rotary.
It is important to remember that the fistula test can be elicited only when vestibular function is retained. Thus, a negative fistula test does not rule out fistula. In fact, the fistula test is positive in less than half of all patients with confirmed fistulae. A false-negative fistula test occurs when the fistula is accompanied by a localized loss of function of the ampulla of the involved canal or by a generalized loss of labyrinthine response. A false-positive fistula test can be seen in the rare condition of a hypermobile stapes without other ear disease. Occasionally, patients with a labyrinthine fistula will experience momentary vertigo when exposed to loud noise, that is, the Tullio phenomenon.
Computed tomographic scanning of the temporal bone is the diagnostic test of choice to rule out cholesteatoma and to evaluate the status of the otic capsule. Labyrinthine fistulae can be readily identified on CT scan, which can help direct surgical management. A fistula of the labyrinth owing to cholesteatoma is an indication for surgery to remove the cholesteatoma and to prevent the retention of infected debris. Fistulae should be managed according to their location, size, and the status of hearing. Even in experienced hands, there is considerable risk to the inner ear in patients with labyrinthine fistula, with rates of total hearing loss between 8 and 56%.8 The conservative management of a labyrinthine fistula consists of a canal.

Acute Petrositis

Petrositis (also known as petrous apicitis) is an inflammation of the petrous portion of the temporal bone. Except for the rather rare acute, fulminating osteomyelitis of the petrosa seen in infants, petrositis occurs only intemporal bones with pneumatic cells in the petrous pyramid. Because less than one-third of petrous bones are pneumatized into the apex, petrositis is an uncommon complication of otitis media. When it does occur, however,petrositis can be a devastating complication. The absence of natural drainage pathways, with a bottleneck to drainage posed by the bony labyrinth that nearly fills the base of the petrous pyramid, and the close proximity to the central nervous system make the petrosa a particularly dangerous site of infection when occupied by virulent organisms. Inflammation of the petrous air cells behaves similarly to that of the mastoid system. Any middle ear infection will result in fluid in pneumatized cells. As in the mastoid process, this inflammation recedes in the great majority of cases as the otitis media subsides without producingsymptoms referable to petrous involvement and without producing bone changes in the cell walls. Such cases are not clinically diagnosed as petrositis. The diagnosis of petrositis is reserved for infected petrous cells with inadequate drainage causing bone changes of coalescence in the cell walls and resulting in symptoms referable to the petrosa.

Although the symptoms of acute petrositis can be subtle, the two most constant complaints are deep-boring pain and aural drainage. The nature of the pain associated with petrositis depends on the area of the petrous pyramid affected. Air cells extend into the petrous pyramid in two main groups: a posterior group of air cells from the epitympanum and antrum that finds its way around the semicircular canals into the base of the pyramid, frequently extending to the apex, and an anterior group of cells from the tympanum, hypotympanum, and eustachian tube that finds its way around the cochlea into the apex of the pyramid. The posterior group of cells is more common and is present in about 30% of temporal bones. In the case of posterior petrositis, the pain is occipital, parietal, or temporal, and the discharge is from the mastoid. In the case of anterior petrositis, the pain is frontal or behind the eye, and the discharge is from the tympanum.

Diplopia caused by sixth cranial nerve paralysis may occur when the apex is involved, the nerve being compressed by edema where it passes through Dorellos canal beneath the petroclinoid (Grubers) ligament at the tip of the petrous apex. The three cardinal symptoms of diplopia (from ipsilateral abducens nerve palsy), retrobulbar pain, and persistent otorrhea constitute Gradenigos syndrome. Yet petrositis often occurs without the full triad. Less common symptoms of petrositis include transient facial nerve paresis, mild recurrent vertigo, and fever that is usually low grade and intermittent.

The diagnosis of petrositis should be suspected whenever there is persistent, purulent discharge and pain, despite a well-done mastoidectomy. The diagnosis is made on clinical suspicion and can usually be confirmed with a high-resolution temporal bone CT scan. Gallium 67 and technetium 99m bone scans are also occasionally helpful, showing increased radioactive uptake on the affected side.

Management of acute petrositis includes parenteral antibiotics and surgical drainage. The object of surgery is to provide adequate drainage from the suppurative focus in the petrosa without damage to either the

Sub-periosteal Abscess

A sub-periosteal abscess is an abscess that forms as a result of either direct destruction of cortical bone or hematogenous spread through small vascular channels. Well-pneumatized mastoids are believed to be more susceptible to forming sub-periosteal abscesses than sclerotic mastoids because of increased capacity for the accumulation of pus and decreased capability of resorption. The most common site of cortex breakdown is through the thin trabecular bone of Macewens triangle. As a result, the auricle is displaced forward and outward, and a fluctuant mass can be palpated behind the ear. When pus breaks through the tip of the mastoid process and into the digastric groove (incisura mastoidea), infection can extend into the neck. This abscess typically forms deep to the sternocleidomastoid muscle and is referred to as a Bezolds abscess. Patients uniformly present with a fluctuant neck mass and otitis media. This infectious process can rapidly prove fatal if left unchecked as the carotid sheath, parapharyngeal space, and mediastinum can all be involved.
Infrequently, purulent secretions can perforate the periosteum and collect deep to the temporalis muscle. When this process occurs from infection tracking alongthe external auditory canal, it is called a Lucs abscess. An alternative and even more uncommon pathway for pus to spread to the temporalis fossa is via a pneumatized zygomatic arch. In either case, patients present with induration and tenderness over the temporalis muscle with projection of the upper half of the pinna awayfrom the calvarium.
Imaging is critical to the diagnosis and management of sub-periosteal abscesses, which occur with relatively low frequency and can present with variable symptoms and signs. Computed tomographic scanning is essential to the detection of a sub-periosteal abscess and to the delineation of the full extent of disease. Although some sub-periosteal abscesses in young children can be managed with intravenous antibiotics and myringotomy alone, treatment generally requires more aggressive surgical intervention. A simple mastoidectomy is first performed to allow drainage and ventilation of the mastoid space.

Intracranial complications

CSF Otorrhea

Drainage of CSF from the ear may be a complication of chronic ear disease or the result of surgery. A frequent cause is a fracture of the temporal bone. Drainage may also develop following irradiation of tumors involving the temporal bone. In rare cases, drainage begins spontaneously without previous ear disease, usually a consequence of a congenital malformation. Regardless of origin, the symptoms, diagnosis, and treatment of CSF otorrhea are the same. Clear, colorless, watery fluid draining from the mastoid cavity or the external auditory canal that reaccumulates immediately after removal by suction or cotton applicator should be assumed to be CSF; however, aspirating clear, watery fluid from the middle ear does not suffice to confirm the diagnosis. The beta transferrin test is conclusive. Initial screening may be accomplished by testing for glucose. Glucose levels in the 60 to 80 mg/100 mL range suggest CSF. The technique used to repair a CSF leak varies with the source, the size of the defect, and the status of the hearing. In general, the goal is to isolate the CSF from the middle ear space, or at least from the eustachian tube orifice, thus preventing retrograde infection and troublesome headaches from decreased CSF pressure. When a CSF leak occurs through a minute dural tear, the dura should be exposed on all sides of the tear. A small graft of temporalis muscle, fascia, or even Gelfoam can usually tamponade the leak. Larger or more extensive tears may require suturing or larger grafts. Acute tears are easier to repair than chronic ones. Defects that are larger than 1 to 2 cm may require an alternate route of repair. Usually, a defect in the middle fossa will require a craniotomy and defect repair from above. Repairs may be completed using muscle, fascia, or bone. A middle fossa defect occurring near the ossicular chain may be small, but repair from above may be necessary to prevent ossicular chain injury. Use of a lumbar drain can reduce pressure on the repair and improve the chances of success.


Generalized bacterial meningitis is defined as an inflammatory response to bacterial infection of the pia-arachnoid and the CSF of the subarachnoid space. Since the subarachnoid space is continuous around the brain, spinal cord, and optic nerves, infections of this space usually involve the entire cerebrospinal axis. Localized meningitis may be defined as a localized inflammation of the dura and pia-arachnoid confined to the region adjacent to a suppurative focus or dural irritation, without viable organisms in the CSF. Meningitis was the most frequent intracranial complication of otitis media in the preantibiotic era.
Otogenic meningitis often goes unrecognized. It is imperative for the physician who is treating a patient with meningitis to rule out a possible otologic cause. Most physicians will suspect an otologic cause in the presence of otorrhea or obvious long-standing ear disease. It is imperative to rule out otitis media in the patient who does not have otorrhea or long-standing otologic complaints.

In patients with suspected meningitis, headache, fever, and neck stiffness are usually present but are not diagnostic. After excluding an intracranial space-occupying complication such as an abscess with CECT scanning of the brain, a lumbar puncture may be performed to confirm the diagnosis. In meningitis, cerebrospinal fluid (CSF) is turbid, usually with raised pressure, pleocytosis, raised protein, low sugar, and low chloride levels. Bacteriologic examination may be positive in untreated cases. Although a brain abscess leaking into the subarachnoid space or subdural empyema may produce a similar CSF picture, the CSF sugar levels are generally not so low. A case of partially treated pyogenic meningitis may occasionally be confused with tuberculous meningitis based on the CSF picture of pleocytosis with lymphocytes predominant. This is a dilemma occasionally faced by us and probably by physicians in other developing countries where tuberculosis is highly prevalent and can manifest as meningitis. The suspicion is heightened if the otoscopic picture is one of CSOM with granulations and no cholesteatoma suggesting tuberculous OM with mastoiditis. Diagnosis here depends on response to appropriate antibiotic therapy and surgical treatment of the mastoid focus. A negative acid-fast bacillus (AFB) smear and culture of both CSF and ear granulations, as well as absence of granulomata on the histopathology of ear granulations, are confirmatory. However, a patient presenting with meningitis and otoscopic evidence of SOM is more likely to have pyogenic rather than tuberculous meningitis. In patients with meningitis following ASOM, particularly if the history of meningitis has been recurrent, it is also important to exclude a congenital inner ear defect such as Mondinis deformity.

Brain Abscess

The early stages of temporal lobe or cerebellar abscess formation produce symptoms of an infective focus with fever, headache, and earache. If antibiotics have been administered, fever is not present. The later stages produce symptoms of raised intracranial pressure and focal neurologic deficit. For a temporal lobe abscess, this includes altered sensorium, homonymous hemianopia, aphasia (if the abscess is left-sided), and facial hemiparesis. For cerebellar abscess, gait ataxia, coarse intention tremor, nystagmus, and past-pointing are typical. The early symptoms of brain abscess may be masked by antibiotics prescribed by a general practitioner. The patient is often not brought to a specialist until the later symptoms and signs appear. Features of concomitant meningitis or lateral sinus thrombosis may predominate while the abscess enlarges; hence, clinical features at this stage are unreliable. CECT scanning of the brain is diagnostic. In brain abscess, the classic ring lesion produced by a hypodense central area (owing to pus) and an enhancing rim (produced by the abscess wall) is characteristically seen. When the abscess capsule has not formed, only hypodense areas with patchy enhancement suggestive of cerebritis or cerebellitis are visible.

Extradural Abscess

Extradural abscesses are a common intracranial complication that may present with earache and increased otorrhea or be asymptomatic and a chance finding at surgery. In CECT scanning of the brain, an extradural abscess is visualized as a hypodense area between the dura and tegmen or between the sinus plate and sigmoid sinus (perisinus abscess). Perisinus abscesses are more common than extradural abscess related to the tegmen.

Subdural Empyema
Patients with subdural empyema present initially with fever and headache similar to patients with brain abscess. However, unlike those with brain abscess, there is rapid progression of symptoms. The onset of seizures, hemiparesis, aphasia, and hemianopia often occurs within a few hours. The patient also appears very toxic. CECT scanning of the brain shows hypodense areas owing to pus collection in the subdural space and is diagnostic.

Lateral Sinus Thrombosis

Persistent fever, otalgia, and neck pain along the upper end of the sternocleidomastoid muscle are the usual features of lateral sinus thrombosis.We rarely encounter patients with isolated lateral sinus thrombosis. Cerebellar abscess and meningitis are the two other complications often occurring concomitantly, and their presence may mask the clinical features of sinus thrombosis. CECT scanning of the brain, if positive, is diagnostic. In lateral sinus thrombosis, the classic delta sign, a triangular area with central hypodensity (owing to the thrombus) and peripheral dural enhancement, may occasionally be seen. The more definitive investigation is MRI. The radiologic findings on MRI are highly variable and depend on the degree of residual flow and the age of the thrombus. In the early or acute phase (first 3 to 5 days) of venous thrombosis, an isointense signal on T1-weighted images and a hypointense signal on T2-weighted images have been described. In the subacute phase (5 to 30 days later), the thrombus becomes hyperintense on T1- and T2-weighted images. In our experience, diagnosis is easily established in the majority of cases by intraoperative findings of discolored dura over the sinus and absence of blood on aspiration of the sinus with a wide-bore needle. Associated perisinus abscess with granulations is commonly seen.


An estimate 100,000 peolpe die annually from the complications of ear disease. The information is not well documented. Please contact Dr. Wagner for further information @ GEO.